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CDC Admits 98 Million Americans Were Given Cancer Virus Via The Polio Shot
#1
Did you get the Polio shot when you were a kid?  I did. Now I'm carrying around a cancer virus that could become active at any time.

Thanks Big Pharma!!   tinyangry

Of course, the article where they admitted this has been removed, but someone took a screenshot before they did... and now we know the truth.   tinyok

#2
Well if its true, it could explain why so many people in there 40s upwards are getting the big C. I just got my anti flu injection today hope its free of any additives tinybighuh
#3
SV40

Quote:SV40

From Wikipedia, the free encyclopedia
[/url][url=https://en.wikipedia.org/wiki/SV40#p-search]
Simian virus 40
[Image: 220px-Symian_virus.png]
Virus classification
Group:
Group I (dsDNA)
Family:
Polyomaviridae
Genus:
Polyomavirus
Species:
Simian virus 40
SV40
Classification and external resources
MeSH
D027601


SV40 is an abbreviation for Simian vacuolating virus 40 or Simian virus 40, a polyomavirus that is found in both monkeys and humans. It was named for the effect it produced on infected green monkey cells, which developed an unusual number of vacuoles. Like other polyomaviruses, SV40 is a DNA virus that has the potential to cause tumors in animals, but most often persists as a latent infection.

The discovery of SV40 revealed that between 1955 and 1963 around 90% of children and 60% of adults in USA were inoculated with SV40-contaminated polio vaccines.[1]

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Historical background[edit]
SV40 was first identified by Ben Sweet and Maurice Hilleman in 1960 when they found that between 10-30% of polio vaccines in the USA were contaminated with SV40.[2] In 1962, Bernice Eddy described the SV40 oncogenic function inducing sarcoma and ependymomas in hamsters inoculated with monkeys cells infected with SV40.[3] The complete viral genome was sequenced by Fiers and his team at the University of Ghent (Belgium) in 1978.[4]

Virology[edit]
SV40 consists of an unenveloped icosahedral virion with a closed circular dsDNA genome[5] of 5.2 kb.[6] The virion adheres to cell surface receptors of MHC class I by the virion glycoprotein VP1. Penetration into the cell is through a caveolin vesicle. Inside the cell nucleus, the cellular RNA polymerase II acts to promote early gene expression. This results in an mRNA that is spliced into two segments. The small and large T antigens result from this. The large T antigen has two functions: 5% goes to the plasma cell membrane and 95% returns to the nucleus. Once in the nucleus the large T antigen binds three viral DNA sites, I, II and III. Binding of sites I and II autoregulates early RNA synthesis. Binding to site II takes place in each cell cycle. Binding site I initiates DNA replication at the origin of replication. Early transcription gives two spliced RNAs that are both 19s. Late transcription gives both a longer 16s, which synthesizes the major viral capsid protein VP1; and the smaller 19s, which gives VP2 and VP3 through leaky scanning. All of the proteins, besides the 5% of large T, return to the nucleus because assembly of the viral particle happens there. Eventual release of the viral particles is cytolytic and results in cell death.[citation needed]

Multiplicity reactivation[edit]
SV40 is capable of multiplicity reactivation (MR).[7][8] MR is the process by which two or more virus genomes containing otherwise lethal damage interact within an infected cell to form a viable virus genome. Yamamato and Shimojo observed MR when SV40 virions were irradiated with UV light and allowed to undergo multiple infection of host cells.[7] Hall studied MR when SV 40 virions were exposed to the DNA crosslinking agent 4, 5’, 8-trimethylpsoralen.[8] Under conditions in which only a single virus particle entered each host cell, approximately one DNA cross-link was lethal to the virus and could not be repaired. In contrast, when multiple viral genomes infected a host cell, psoralen-induced DNA cross-links were repaired; that is, MR occurred. Hall suggested that the virions with cross-linked DNA were repaired by recombinational repair.[8] Michod et al. reviewed numerous examples of MR in different viruses and suggested that MR is a common form of sexual interaction that provides the advantage of recombinational repair of genome damages.[9]

Transcription[edit]
The early promoter for SV40 contains three elements. The TATA box is located approximately 20 base-pairs upstream from the transcriptional start site. The 21 base-pair repeats contain six GC boxes and are the site that determines the direction of transcription. Also, the 72 base-pair repeats are transcriptional enhancers. When the SP1 protein interacts with the 21 bp repeats it binds either the first or the last three GC boxes. Binding the first three initiates early expression and binding the last three initiates late expression. The function of the 72 bp repeats is to enhance the amount of stable RNA and increase the rate of synthesis. This is done by binding (dimerization) with the AP1 (activator protein 1) to give a primary transcript that is 3' polyadenylated and 5' capped.[citation needed]
SV40 in animals[edit]

SV40 is dormant and is asymptomatic in rhesus monkeys. The virus has been found in many macaque populations in the wild, where it rarely causes disease. However, in monkeys that are immunodeficient—due to, for example, infection with Simian immunodeficiency virus—SV40 acts much like the human JC and BK polyomaviruses, producing kidney disease and sometimes a demyelinating disease similar to PML. In other species, particularly hamsters, SV40 causes a variety of tumors, generally sarcomas. In rats, the oncogenic SV40 large T-antigen was used to establish a brain tumor model for PNETs and medulloblastomas.[10]

The molecular mechanisms by which the virus reproduces and alters cell function were previously unknown, and research into SV40 vastly increased biologists' understanding of gene expression and the regulation of cell growth.[citation needed]

Hypothesized role in human disease[edit]
The hypothesis that SV40 might cause cancer in humans has been a particularly controversial area of research.[11] Several methods have detected SV40 in a variety of human cancers, although how reliable these detection methods are, and whether SV40 has any role in causing these tumors, remains unclear.[12] As a result of these uncertainties, academic opinion remains divided, with some arguing that this hypothesis is not supported by the data[13] and others arguing that some cancers may involve SV40.[14][15] The US National Cancer Institute announced in 2004 that although SV40 does cause cancer in some animal models, "substantial epidemiological evidence has accumulated to indicate that SV40 likely does not cause cancer in humans".[16] This announcement was based on two studies.[17][18] This 2004 announcement is in contrast to a 2002 study performed by The National Academy of Sciences Immunization Safety Review committee that stated, "The committee concludes that the biological evidence is moderate that SV40 exposure could lead to cancer in humans under natural conditions.”[19] However, Namika, Goodison,...and Rosser found that the SV40 large t-antigen, in combination with mycoplasma, often a contaminate of vaccines, can cause prostate cells to turn cancerous. Whether or not this is true for other human cells is debated.[20]

p53 damage and carcinogenicity[edit]

SV40 is believed to suppress the transcriptional properties of the tumor-suppressing p53 in humans through the SV40 large T-antigen and SV40 small T-antigen. p53 is responsible for initiating regulated cell death ("apoptosis"), or cell cycle arrest when a cell is damaged. A mutated p53 gene may contribute to uncontrolled cellular proliferation, leading to a tumor.

SV40 may act as a co-carcinogen with crocidolite asbestos to cause both Peritoneal and Pleural Mesothelioma.[21][22]
When SV40 infects nonpermissive cells, such as 3T3 mouse cells, the dsDNA of SV40 becomes covalently integrated. In nonpermissive cells only early gene expression occurs and this leads to transformation, or oncogenesis. The nonpermissive host needs the large T-antigen and the small t-antigen in order to function. The small T-antigen interacts with and integrates with the cellular phosphatase pp2A. This causes the cell to lose the ability to initiate transcription.[citation needed]

Polio vaccine contamination[edit]

Soon after its discovery, SV40 was identified in the oral form of the polio vaccine produced between 1955 and 1961 by American Home Products (dba Lederle). This is believed to be due to two sources: 1) SV40 contamination of the original seed strain (coded SOM); 2) contamination of the substrate—primary kidney cells from infected monkeys used to grow the vaccine virus during production. Both the Sabin vaccine (oral, live virus) and the Salk vaccine (injectable, killed virus) were affected; the technique used to inactivate the polio virus in the Salk vaccine, by means of formaldehyde, did not reliably kill SV40. The contaminated vaccine continued to be distributed to the public through 1963.[23][24]
It was difficult to detect small quantities of virus until the advent of PCR; since then, stored samples of vaccine made after 1962 have tested negative for SV40. In 1997, Herbert Ratner of Oak Park, Illinois, gave some vials of 1955 Salk vaccine to researcher Michele Carbone.[25] Ratner, the Health Commissioner of Oak Park at the time the Salk vaccine was introduced, had kept these vials of vaccine in a refrigerator for over forty years.[26][27] Upon testing this vaccine, Carbone discovered that it contained not only the SV40 strain already known to have been in the Salk vaccine (containing two 72-bp enhancers) but also the same slow-growing SV40 strain currently found in some malignant tumors and lymphomas (containing one 72-bp enhancers).[28] It is unknown how widespread the virus was among humans before the 1950s, though one study found that 12% of a sample of German medical students in 1952 had SV40 antibodies.[29]

An analysis presented at the Vaccine Cell Substrate Conference in 2004[30] suggested that vaccines used in the former Soviet bloc countries, China, Japan, and Africa, could have been contaminated up to 1980, meaning that hundreds of millions more could have been exposed to the virus unknowingly.

Population level studies show no evidence of any increase in cancer incidence as a result of exposure,[31] though SV40 has been extensively studied.[32] A thirty-five year followup found no excess of the cancers putatively associated with SV40.[33]

See also[edit]
#4
Green Monkey

Quote:Green monkey

From Wikipedia, the free encyclopedia
[/url]
This article is about the primate of the family Cercopithecidae. For other uses, see Green monkey (disambiguation).
Green monkey[1]
[Image: 220px-Green_monkey_%28Chlorocebus_sabaeu...e_head.jpg]
juvenile, Gambia


[Image: 220px-Status_iucn3.1_LC.svg.png]
Least Concern (IUCN 3.1)[2]
Scientific classification
Kingdom:
Animalia
Phylum:
Chordata
Class:
Mammalia
Order:
Primates
Family:
Cercopithecidae
Genus:
Chlorocebus
Species:
C. sabaeus
Binomial name
Chlorocebus sabaeus
(Linnaeus1758)
[Image: 200px-Chlorocebus_sabaeus_distribution.svg.png]
Geographic range
The green monkey (Chlorocebus sabaeus), also known as the sabaeus monkey or the callithrix monkey,[3] is an Old World monkey with golden-green fur and pale hands and feet.[4] The tip of the tail is golden yellow as are the backs of the thighs and cheek whiskers.[4] It does not have a distinguishing band of fur on the brow, like other Chlorocebus species, and males have a pale blue scrotum.[4] Some authorities consider this and all of the members of the genus Chlorocebus to be a single widespread species, Chlorocebus aethiops.


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Physical description[edit]
The green monkey is a sexually dimorphic species, with males typically being slightly larger than females. Wild adult males weigh between 3.9 and 8.0 kg (8.6 and 17.6 lb) and measure between 420 and 600 mm (1.38 and 1.97 ft), while the females usually weigh between 3.4 and 5.3 kg (7.5 and 11.7 lb) and measure between 300 and 495 mm (0.984 and 1.624 ft).[4]


Habitat and distribution[edit]
Callithrix monkeys can be found in a wide range of wooded habitats, ranging from very dry Sahel woodland to the edge of rainforests. It is also commonly seen in coastal regions, where known to feed on seashore foods such as crabs.[3] It also takes a wide variety of other foods, including fruits and invertebrates.[3]

The green monkey is found in West Africa from Senegal to the Volta River. It has been introduced to the Cape Verde islands off north-western Africa, and the West Indian islands of Saint KittsNevisSaint Martin, and Barbados.[1] It was introduced to the West Indies in the late 17th century when slave trade ships traveled to the Caribbean from West Africa.[4]
Behavior[edit]
[Image: 220px-Chlorocebus_perspective.jpg]


Skull of male

As other members of the genus Chlorocebus, the green monkey is highly social and usually seen in groups. They usually live in groups of up to 7 to 80 individuals. Within these groups, there is distinct social hierarchy evidenced by grooming behaviors and gender relationships.

Green monkeys are known to communicate both verbally and non-verbally. They have distinct calls which they use to warn others in the group of predators, and even have specific calls for specific predators. Body language, such as the display of brightly colored genitalia is also used to communicate danger, but can also be used as a way of establishing dominance. It has also been documented that green monkeys may use facial expressions to express their emotional state.[5]

Reproduction[edit]

[Image: 220px-Chlorocebus_sabaeus_0024.jpg]


Adult

Green monkeys live in a polygynous society, revolving around the alpha males. The alpha males have control over social interactions and mating between other males and females in the group.

These monkeys are seasonal breeders, breeding during the April to June months (October and November in the Nyes area North West of Thies), during which rainfall is the heaviest. It is during these rainy seasons that fruit is most abundant, so it is speculated that green monkeys schedule their breeding around this time, when resources are most abundant. They breed about once a year, with males reaching sexual maturity in 5 years, females in 2. Despite infant mortality being fairly high, at roughly 57%, green monkeys are known to be heavily invested in their offspring, with mothers taking care of their young for about a year before letting them venture out as individual adults.

References[edit]
[Image: 30px-Commons-logo.svg.png]
Wikimedia Commons has media related to Green monkey.

  1. Jump up to:a b Groves, C.P. (2005). Wilson, D.E.; Reeder, D.M., eds. Mammal Species of the World: A Taxonomic and Geographic Reference (3rd ed.). Baltimore: Johns Hopkins University Press. pp. 158–159. ISBN 0-801-88221-4OCLC 62265494.

  2. Jump up^ Kingdon, J. & Gippoliti, S. (2008). "Chlorocebus sabaeus"IUCN Red List of Threatened Species. Version 2008International Union for Conservation of Nature. Retrieved 4 January 2009.

  3. Jump up to:a b c Kingdon, J. (1997). The Kingdon Guide to African Mammals. London: Academic Press Limited. ISBN 0-12-408355-2.[page needed]

  4. Jump up to:a b c d e Cawthon Lang, K. A. (2006). "Primate Factsheets: Vervet (Chlorocebus) Taxonomy, Morphology, & Ecology". Retrieved 2007-08-13.

  5. Jump up^ Matthew Keller, [1], "Animal Diversity Web", 3/26/12


Extant species of family Cercopithecidae (Old World monkeys) (subfamily Cercopithecinae)

External links[edit]

and

Rhesus_macaque

Quote:Rhesus macaque

From Wikipedia, the free encyclopedia

For other uses, see Rhesus (disambiguation).
Rhesus macaque
[Image: 220px-Macaca_mulatta_in_Guiyang.jpg]


[Image: 220px-Status_iucn3.1_LC.svg.png]
Least Concern (IUCN 3.1)[1]
Scientific classification
Kingdom:
Animalia
Phylum:
Chordata
Class:
Mammalia
Order:
Primates
Family:
Cercopithecidae
Genus:
Macaca
Species:
M. mulatta
Binomial name
Macaca mulatta[2]
(Zimmermann, 1780)
[Image: 220px-Rhesus_Macaque_area.png]
Rhesus macaque native range
Synonyms[3]

Species synonymy [show]

[Image: 220px-Indochinese_Rhesus_Macaque.jpg]


Indochinese Rhesus Macaque (Macaca mulatta siamica) from Monkey Island, Cat ba National Park, Vietnam

The rhesus macaque (Macaca mulatta) is one of the best-known species of Old World monkeys. It is listed as Least Concern in the IUCN Red List of Threatened Species in view of its wide distribution, presumed large population, and its tolerance of a broad range of habitats. Native to SouthCentral, and Southeast Asia, rhesus macaque troops inhabit a great variety of habitats, from grasslands to arid and forested areas, but also close to human settlements.[1]

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Characteristics[edit]
The rhesus macaque is brown or grey in color and has a pink face, which is bereft of fur. Its tail is of medium length and averages between 20.7 and 22.9 cm (8.1 and 9.0 in). Adult males measure about 53 cm (21 in) on average and weigh about 7.7 kg (17 lb). Females are smaller, averaging 47 cm (19 in) in length and 5.3 kg (12 lb) in weight. Rhesus macaques have, on average, 50 vertebrae. Their ratio of arm length to leg length is 89%. They have dorsal scapulae and a wide rib cage.

The rhesus macaque has 32 teeth with a dental formula of 2.1.2.3/2.1.2.3 and bilophodont molars. The upper molars have four cuspsparaconemetaconeprotocone, and hypocone. The lower molars also have four cusps: metaconidprotoconidhypoconid, and entoconid.

Distribution and habitat[edit]
Rhesus macaques are native to IndiaBangladeshPakistanNepalBurmaThailandAfghanistanVietnam, southern China, and some neighboring areas. They have the widest geographic ranges of any nonhuman primate, occupying a great diversity of altitudes throughout Central, South, and Southeast Asia. Inhabiting arid, open areas, rhesus macaques may be found in grasslands, woodlands, and in mountainous regions up to 2,500 m (8,200 ft) in elevation. They are regular swimmers. Babies as young as a few days old can swim, and adults are known to swim over a half mile between islands, but are often found drowned in small groups where their drinking waters lie.[citation needed] Rhesus macaques are noted for their tendency to move from rural to urban areas, coming to rely on handouts or refuse from humans.[4] They adapt well to human presence, and form larger troops in human-dominated landscapes than in forests.[5]

The southern and the northern distributional limits for rhesus and bonnet macaques, respectively, currently run parallel to each other in the western part of India, are separated by a large gap in the center, and converge on the eastern coast of the peninsula to form a distribution overlap zone. This overlap region is characterized by the presence of mixed-species troops, with pure troops of both species sometimes occurring even in close proximity to one another. The range extension of rhesus macaque – a natural process in some areas, and a direct consequence of introduction by humans in other regions – poses grave implications for the endemic and declining populations of bonnet macaques in southern India.[6][7]

The Thai population is locally classified as endangered. There are about 1,000 troops at Wat Tham Pha Mak Ho, Tambon Si Songkhram, Wang Saphung districtLoei province.[8]
Distribution of subspecies and populations[edit]
[Image: 220px-Macaque_India_4.jpg]


Rhesus macaques in the Red Fort of Agra in India

[Image: 220px-Rhesus_Macaque_%28Macaca_mulatta%2...G_5792.jpg]


Rhesus macaque in Kinnerasani Wildlife SanctuaryAndhra Pradesh, India

The name "rhesus" is reminiscent of the Greek mythological king, Rhesus. However, the French naturalist Jean-Baptiste Audebert, who applied the name to the species, stated: "it has no meaning".[9]

According to Zimmermann’s first description of 1780, the rhesus macaque is distributed in eastern AfghanistanBangladeshBhutan, as far east as the Brahmaputra Valley in peninsular IndiaNepal, and northern Pakistan. Today, this is known as the Indian rhesus macaque M. m. mulatta, which includes the morphologically similar M. rhesus villosus, described by True in 1894, from Kashmir, and M. m. mcmahoni, described by Pocock in 1932 from Kootai, Pakistan. Several Chinese subspecies of rhesus macaques were described between 1867 and 1917. The molecular differences identified among populations, however, are alone not consistent enough to conclusively define any subspecies.[10]

The Chinese subspecies can be divided as follows:
  • M. m. mulatta is found in western and central China, in the south of Yunnan, and southwest of Guangxi;[11]
  • M. m. lasiota (Gray, 1868), the west Chinese rhesus macaque, is distributed in the west of Sichuan, northwest of Yunnan, and southeast of Qinghai;[11] it is possibly synonymous with M. m. sanctijohannis (Swinhoe, 1867), if not with M. m. mulatta.[10]
  • M. m. tcheliensis (Milne-Edwards, 1870), the north Chinese rhesus macaque, lives in the north of Henan, south of Shanxi, and near Beijing. Some consider it as the most endangered subspecies.[12] Others consider it possibly synonymous with M. m. sanctijohannis, if not with M. m. mulatta.[10]
  • M. m. vestita (Milne-Edwards, 1892), the Tibetan rhesus macaque, lives in the southeast of Tibet, northwest of Yunnan (Deqing), and perhaps including Yushu;[11] it is possibly synonymous with M. m. sanctijohannis, if not with M. m. mulatta.[10]
  • M. m. littoralis (Elliot, 1909), the south Chinese rhesus macaque, lives in FujianZhejiangAnhuiJiangxiHunanHubeiGuizhou, northwest of Guangdong, north of Guangxi, northeast of Yunnan, east of Sichuan, and south of Shaanxi;[11] it is possibly synonymous with M. m. sanctijohannis, if not with M. m. mulatta.[10]
  • M. m. brevicaudus, also referred to as Pithecus brevicaudus (Elliot, 1913), lives on the Hainan Island and Wanshan Islands in Guangdong, and the islands near Hong Kong;[11] it may be synonymous with M. m. mulatta.[10]
  • M. m. siamica (Kloss, 1917), the Indochinese rhesus macaque, is distributed in Myanmar, in the north of Thailand and Vietnam, in Laos, and in the Chinese provinces of Anhui, northwest Guangxi, Guizhou, HubeiHunan, central and eastern Sichuan, and western and south-central Yunnan; possibly synonymous with M. m. sanctijohannis, if not with M. m. mulatta.[10]

Feral colonies in the United States[edit]
Main article: feral rhesus macaque
Around the spring of 1938, a colony of rhesus macaques called "the Nazuris" was released in and around Silver Springs in Florida by a tour boat operator known locally as "Colonel Tooey" to enhance his "Jungle Cruise". A traditional story that the monkeys were released for scenery enhancement in the Tarzan movies that were filmed at that location is false, as the only Tarzan movie filmed in the area, 1939's Tarzan Finds a Son!, does not contain rhesus macaques.[13] In addition, various colonies of rhesus and other monkey species are speculated to be the result of zoos and wildlife parks destroyed in hurricanes, most notably Hurricane Andrew.[14]

A notable colony of rhesus macaques on Morgan Island, one of the Sea Islands in the South Carolina Lowcountry, was imported in the 1970s for use in local labs and are, by all accounts, thriving.[15]

Ecology and behavior[edit]
[Image: 220px-Rhesus_band_rishikesh_india2008.jpg]


A roadside band of rhesus macaque in RishikeshUttarakhandIndia: Although they are infamous as urban pests, which are quick to steal not only food, but also household items, it is not certain if the pair of jeans draped over the wall on the right is their handiwork.

Rhesus macaques are diurnal animals, and both arboreal and terrestrial. They are quadrupedal and, when on the ground, they walk digitigrade and plantigrade. They are mostly herbivorous, feeding mainly on fruit, but also eating seedsrootsbudsbark, and cereals. They are estimated to consume around 99 different plant species in 46 families. During the monsoon season, they get much of their water from ripe and succulent fruit. Macaques living far from water sources lick dewdrops from leaves and drink rainwater accumulated in tree hollows.[16] They have also been observed eating termitesgrasshoppersants, and beetles.[17] When food is abundant, they are distributed in patches, and forage throughout the day in their home ranges. They drink water when foraging, and gather around streams and rivers.[18]Rhesus macaques have specialized pouch-like cheeks, allowing them to temporarily hoard their food.

In psychological research, rhesus macaques have demonstrated a variety of complex cognitive abilities, including the ability to make same-different judgments, understand simple rules, and monitor their own mental states.[19][20] They have even been shown to demonstrate self-agency,[21] an important type of self-awareness. In 2014, onlookers at a train station in Kanpur, India, documented a rhesus monkey, knocked unconscious by overhead power lines, that was revived by another rhesus that systematically administered a series of resuscitative actions.[22]

Group structure[edit]
Like other macaques, rhesus troops comprise a mixture of 20–200 males and females.[23] Females may outnumber the males by a ratio of 4:1. Males and females both have separate hierarchies. Female philopatry, common among social mammals, has been extensively studied in rhesus macaques. Females tend not to leave the social group, and have highly stable matrilineal hierarchies in which a female’s rank is dependent on the rank of her mother. In addition, a single group may have multiple matrilineal lines existing in a hierarchy, and a female outranks any unrelated females that rank lower than her mother.[24] Rhesus macaques are unusual in that the youngest females tend to outrank their older sisters.[25] This is likely because young females are more fit and fertile. Mothers seem to prevent the older daughters from forming coalitions against her.[clarification needed] The youngest daughter is the most dependent on the mother, and would have nothing to gain from helping her siblings in overthrowing their mother. Since each daughter had a high rank in her early years, rebelling against her mother is discouraged.[26]Juvenile male macaques also exist in matrilineal lines, but once they reach four to five years of age, they are driven out of their natal groups by the dominant male. Thus, adult males gain dominance by age and experience.[18]

In the group, macaques position themselves based on rank. The "central male subgroup" contains the two or three oldest and most dominant males which are codominant, along with females, their infants, and juveniles. This subgroup occupies the center of the group and determines the movements, foraging, and other routines.[18] The females of this subgroup are also the most dominant of the entire group. The farther to the periphery a subgroup is, the less dominant it is. Subgroups on the periphery of the central group are run by one dominant male, of a rank lower than the central males, and he maintains order in the group, and communicates messages between the central and peripheral males. A subgroup of subordinate, often subadult, males occupy the very edge of the groups, and have the responsibility of communicating with other macaque groups and making alarm calls.[27] Rhesus social behaviour has been described as despotic, in that high-ranking individuals show little tolerance and frequent and often severe aggression towards non-kin.[28]

Communication[edit]
Rhesus macaques interact using a variety of facial expressions, vocalizations, body postures, and gestures. Perhaps the most common facial expression the macaque makes is the "silent bared teeth" face.[29] This is made between individuals of different social ranks, with the lower-ranking one giving the expression to its superior. A less-dominant individual also makes a "fear grimace", accompanied by a scream, to appease or redirect aggression.[30] Another submissive behavior is the "present rump", where an individual raises its tail and exposes its genitals to the dominant one.[29] A dominant individual threatens another individual by standing quadrupedally and making a silent "open mouth stare" accompanied by the tail sticking straight.[31] During movements, macaques make coos and grunts. These are also made during affiliative interactions, and approaches before grooming.[32] When they find rare food of high quality, macaques emit warbles, harmonic arches, or chirps. When in threatening situations, macaques emit a single loud, high-pitched sound called a shrill bark.[33] Screeches, screams, squeaks, pant-threats, growls, and barks are used during aggressive interactions.[33] Infants "gecker" to attract their mother's attention.[34]

Reproduction[edit]
[Image: 220px-Macaca_mulatta_3.JPG]


Rhesus macaque with two babies near the Jakhu temple of ShimlaHimachal Pradesh

Adult male macaques try to maximize their reproductive success by entering into sex with females, both in and outside the breeding period. Females prefer to mate with males that will increase the survival of their young. Thus, a consort male provides resources for his female and protects her from predators. Larger, more dominant males are more likely to provide for the females. The breeding period can last up to 11 days, and a female usually mates with four males during that time. Male rhesus macaques have not been observed to fight for access to sexually receptive females, although they suffer more wounds during the mating season.[35] Female macaques first breed when they are four years old, and reach menopause at around 25 years of age.[36] When mating, a male rhesus monkey usually ejaculates less than 15 seconds after sexual penetration.[37] Male macaques generally play no role in raising the young, but do have peaceful relationships with the offspring of their consort pairs.[18]

Manson and Parry[38] found that free-ranging rhesus macaques avoid inbreeding. Adult females were never observed to copulate with males of their own matrilineage during their fertile periods.

Mothers with one or more immature daughters in addition to their infants are in contact with their infants less than those with no older immature daughters, because the mothers may pass the parenting responsibilities to their daughters. High-ranking mothers with older immature daughters also reject their infants significantly more than those without older daughters, and tend to begin mating earlier in the mating season than expected based on their dates of parturition the preceding birth season.[39] Infants farther from the center of the groups are more vulnerable to infanticide from outside groups.[18] Some mothers abuse their infants, which is believed to be the result of controlling parenting styles.[40]

Self-awareness[edit]
In several experiments giving mirrors to rhesus monkeys, they looked into the mirrors and groomed themselves as well as flexed various muscle groups. This behaviour indicates that they recognised and were aware of themselves.[41]
In science[edit]
[Image: 220px-Sam_prior_to_Little_Joe_2_-_C-1959-52201.jpg]


[url=https://en.wikipedia.org/wiki/Project_Mercury]Project Mercury rocket Little Joe 1B, launched in 1960, carried Miss Sam to 9.3 mi (15.0 km) in altitude.

The rhesus macaque is well known to science. Due to its relatively easy upkeep in captivity, wide availability, and closeness to humans anatomically and physiologically, it has been used extensively in medical and biological research on human and animal health-related topics. It has given its name to the Rh factor, one of the elements of a person's blood group, by the discoverers of the factor, Karl Landsteiner and Alexander Wiener. The rhesus macaque was also used in the well-known experiments on maternal deprivation carried out in the 1950s by controversial comparative psychologist Harry Harlow. Other medical breakthroughs facilitated by the use of the rhesus macaque include:

The U.S. Army, the U.S. Air Force, and NASA launched rhesus macaques into outer space during the 1950s and 1960s, and the Soviet/Russian space program launched them into space as recently as 1997 on the Bion missions. One of these primates ("Able"), which was launched on a suborbital spaceflight in 1959, was among the first living beings (along with "Miss Baker" on the same mission) to travel in space and return alive.[43]
On October 25, 1999, the rhesus macaque became the first cloned primate with the birth of Tetra. January 2001 had the birth of ANDi, the first transgenic primate; ANDi carries foreign genes originally from a jellyfish.[44]

Though most studies of the rhesus macaque are from various locations in northern India, some knowledge of the natural behavior of the species comes from studies carried out on a colony established by the Caribbean Primate Research Center of the University of Puerto Ricoon the island of Cayo Santiago, off Puerto Rico.[citation needed] No predators are on the island, and humans are not permitted to land except as part of the research programmes. The colony is provisioned to some extent, but about half of its food comes from natural foraging.

Rhesus macaques, like many macaques, carry the herpes B virus. This virus does not typically harm the monkey, but is very dangerous to humans in the rare event that it jumps species, for example in the 1997 death of Yerkes National Primate Research Center researcher Elizabeth Griffin.[45][46][47]

Sequencing the genome[edit]
Genomic informationNCBI genome ID
215
Ploidy
diploid
Genome size
3,097.37 Mb
Number of chromosomes
21 pairs
Year of completion
2007
Work on the genome of the rhesus macaque was completed in 2007, making the species the second nonhuman primate to have its genome sequenced.[48] Humans and macaques apparently share about 93% of their DNA sequence and shared a common ancestorroughly 25 million years ago.[49] The rhesus macaque has 21 pairs of chromosomes.[50]

Comparison of rhesus macaques, chimpanzees, and humans revealed the structure of ancestral primate genomes, positive selection pressure and lineage-specific expansions, and contractions of gene families.

"The goal is to reconstruct the history of every gene in the human genome," said Evan Eichler, University of Washington, Seattle. DNA from different branches of the primate tree will allow us "to trace back the evolutionary changes that occurred at various time points, leading from the common ancestors of the primate clade to Homo sapiens," said Bruce Lahn, University of Chicago.[51]

After the human and chimpanzee genomes were sequenced and compared, it was usually impossible to tell whether differences were the result of the human or chimpanzee gene changing from the common ancestor. After the rhesus macaque genome was sequenced, three genes could be compared. If two genes were the same, they were presumed to be the original gene.[52]

The chimpanzee and human genome diverged 6 million years ago. They have 98% identity and many conserved regulatory regions. Comparing the macaque and human genomes, which diverged 25 million years ago and had 93% identity, further identified evolutionary pressure and gene function.

Like the chimpanzee, changes were on the level of gene rearrangements rather than single mutations. Frequent insertions, deletions, changes in the order and number of genes, and segmental duplications near gaps, centromeres and telomeres occurred. So, macaque, chimpanzee, and human chromosomes are mosaics of each other.

Surprisingly, some normal gene sequences in healthy macaques and chimpanzees cause profound disease in humans. For example, the normal sequence of phenylalanine hydroxylase in macaques and chimpanzees is the mutated sequence responsible for phenylketonuria in humans. So, humans must have been under evolutionary pressure to adopt a different mechanism.

Some gene families are conserved or under evolutionary pressure and expansion in all three primate species, while some are under expansion uniquely in human, chimpanzee, or macaque.

For example, cholesterol pathways are conserved in all three species (and other primate species). In all three species, immune response genes are under positive selection, and genes of T cell-mediated immunity, signal transduction, cell adhesion, and membrane proteins generally. Genes for keratin, which produce hair shafts, were rapidly evolving in all three species, possibly because of climate change or mate selection. The X chromosome has three times more rearrangements than other chromosomes. The macaque gained 1,358 genes by duplication.
Triangulation of human, chimpanzee, and macaque sequences showed expansion of gene families in each species.
The PKFP gene, important in sugar (fructose) metabolism, is expanded in macaques, possibly because of their high-fruit diet. So are genes for the olfactory receptor, cytochrome P450 (which degrades toxins), and CCL3L1-CCL4 (associated in humans with HIV susceptibility).

Immune genes are expanded in macaques, relative to all four great ape species. The macaque genome has 33 major histocompatibility genes, three times those of human. This has clinical significance because the macaque is used as an experimental model of the human immune system.

In humans, the preferentially expressed antigen of melanoma (PRAME) gene family is expanded. It is actively expressed in cancers, but normally is testis-specific, possibly involved in spermatogenesis. The PRAME family has 26 members on human chromosome 1. In the macaque, it has eight, and has been very simple and stable for millions of years. The PRAME family arose in translocations in the common mouse-primate ancestor 85 million years ago, and is expanded on mouse chromosome 4.

DNA microarrays are used in macaque research. For example, Michael Katze of University of Washington, Seattle, infected macaques with 1918 and modern influenzas. The DNA microarray showed the macaque genomic response to human influenza on a cellular level in each tissue. Both viruses stimulated innate immune system inflammation, but the 1918 flu stimulated stronger and more persistent inflammation, causing extensive tissue damage, and it did not stimulate the interferon-1 pathway. The DNA response showed a transition from innate to adaptive immune response over seven days.[53][54]

The full sequence and annotation of the macaque genome is available on the Ensembl genome browser.
See also[edit]


It means something very nasty

It indicates a vector for the source of AIDs as well.. 
Long story but my research from years ago..

It is best described as a crime against humanity
#5
That was one hell of a read, thank you. It will take me a long time to digest it all
#6
But wait, There's more tinywhat


Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer


Quote:
Quote:Clin Microbiol Rev. 2004 Jul; 17(3): 495–508.
doi:  10.1128/CMR.17.3.495-508.2004
PMCID: PMC452549

Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer
Regis A. Vilchez1,2 and Janet S. Butel2,*
Author information ► Copyright and License information ►

This article has been cited by other articles in PMC.




ABSTRACT
The polyomavirus simian virus 40 (SV40) is a known oncogenic DNA virus which induces primary brain and bone cancers, malignant mesothelioma, and lymphomas in laboratory animals. Persuasive evidence now indicates that SV40 is causing infections in humans today and represents an emerging pathogen. A meta-analysis of molecular, pathological, and clinical data from 1,793 cancer patients indicates that there is a significant excess risk of SV40 associated with human primary brain cancers, primary bone cancers, malignant mesothelioma, and non-Hodgkin's lymphoma. Experimental data strongly suggest that SV40 may be functionally important in the development of some of those human malignancies. Therefore, the major types of tumors induced by SV40 in laboratory animals are the same as those human malignancies found to contain SV40 markers. The Institute of Medicine recently concluded that “the biological evidence is of moderate strength that SV40 exposure could lead to cancer in humans under natural conditions.” This review analyzes the accumulating data that indicate that SV40 is a pathogen which has a possible etiologic role in human malignancies. Future research directions are considered.


INTRODUCTION
The polyomavirus simian virus 40 (SV40) is a potent DNA tumor virus, and mounting evidence suggests that it is an emergent human pathogen (110121339495066111123). Recently, the Institute of Medicine of the National Academies concluded that “the biological evidence is strong that SV40 is a transforming virus” and that “the biological evidence is of moderate strength that SV40 exposure could lead to cancer in humans under natural conditions” (111). In addition, two other independent scientific panels have made similar conclusions (53131). A recent analysis suggested that SV40 should be included in the list of group 2A carcinogens (i.e., agents for which evidence is indicative but not definitive for carcinogenesis in humans) by the International Agency for Research on Cancer (39). Therefore, as SV40 is recognized as a potent oncogenic agent, it is important to evaluate the increasing data that implicate the virus in some human malignancies. This review examines the biological, pathological and clinical evidence of SV40 pathogenesis and discusses future directions needed to define an etiologic role for the virus in some of these devastating diseases.

History of SV40 Contamination of Polio Vaccines
The discovery of the polyomavirus SV40, as well as its introduction as a pathogen into the human population, was tied to the development and worldwide distribution of early forms of the polio vaccine (1395111123). Inactivated (Salk) and early live attenuated (Sabin) forms of polio vaccines were inadvertently contaminated with SV40 (9597111). In addition, different adenovirus vaccines distributed to some U.S. military personnel from 1961 to 1965 also contained SV40 (64). The viral contamination occurred because these early vaccines were prepared in primary cultures of kidney cells derived from rhesus monkeys, which are often naturally infected with SV40 (1395111). Infectious SV40 survived the vaccine inactivation treatments, and conservative estimates indicate that up to 30 million people (children and adults) in the United States may have been exposed to live SV40 from 1955 through 1963 when administered potentially contaminated polio vaccines (95111). Millions of people worldwide were also potentially exposed to SV40 because contaminated polio vaccines were distributed and used in many countries (85123). These data led the Institute of Medicine to conclude that “the biological evidence is of moderate strength that SV40 exposure from the polio vaccine is related to SV40 infection in humans” (111).

Shortly after its discovery, SV40 was shown to be a potent oncogenic DNA virus (13). In animal models, the neoplasias induced by SV40 included primary brain cancers, malignant mesotheliomas, bone tumors, and systemic lymphomas (13). Subsequently, many in vitro studies established that the oncogenic capacity of SV40 reflects the disruption of critical cell cycle control pathways (996116). During the last decade, numerous published studies from independent laboratories, using different molecular biology techniques, have demonstrated SV40 large tumor antigen (T-ag) or DNA in primary human brain and bone cancers and malignant mesothelioma (1133950123). More recently, studies have demonstrated that SV40 T-ag sequences are significantly associated with non-Hodgkin's lymphoma (NHL) (102124125). Therefore, the major types of tumors induced by SV40 in laboratory animals are the same as those human malignancies found to contain SV40 markers. A recent meta-analysis (122) of the molecular evidence conclusively established a significant excess risk of SV40 with those selected human cancers.

It is noteworthy that SV40 has been detected in malignancies from children and young adults not exposed to contaminated polio vaccines, as well as in older adults (518717376117124125129132133). The detection of viral markers in young persons, by using molecular techniques, coupled with the isolation of infectious SV40 from tumors (62) and from nonneoplastic specimens (6667), suggests that SV40 continues to cause infections in the human population today. In contrast, some retrospective epidemiological studies have failed to demonstrate an increased cancer risk in populations which had a high likelihood of having received potentially contaminated polio vaccine (208295112114). However, the epidemiological data available are recognized to be inconclusive and limited (95111123), and the Institute of Medicine found that the epidemiological data for cancer rates in people potentially exposed to SV40-contaminated vaccines are inadequate to evaluate a causal relationship (111). This conclusion is based on the lack of data on which individuals actually received contaminated vaccines, the unknown dosage of infectious SV40 present in particular lots of vaccine, the failure to know who among the exposed were successfully infected with SV40, the inability to know if the vaccine “unexposed” cohorts may have been exposed to SV40 from other sources, and the difficulty of monitoring a large population for cancer development for years after virus exposure. These important limiting factors led the Institute of Medicine to “not recommend additional epidemiological studies of people potentially exposed to contaminated polio vaccine.”


VIROLOGY AND PATHOGENESIS OF INFECTIONS
Properties of the Virus
SV40 is in the family Polyomaviridae, which includes JC virus (JCV) and BK virus (BKV). Polyomaviruses are small, nonenveloped, icosahedral DNA viruses. Their genomes consist of a single copy of double-stranded, circular, supercoiled DNA about 5 kb in length. BKV and JCV share 72% DNA sequence homology, and each shares approximately 70% homology with SV40. Although these viruses are related, they can be distinguished easily at the DNA and protein levels. Genetic differences, particularly in the noncoding, regulatory regions of the viral genomes, may determine important differences in host range. Furthermore, the three viruses can be differentiated serologically by neutralization and hemagglutination assays (525698).

The SV40 genome is divided into early and late regions, with the early region coding for the large and small T-ags and the late region encoding the capsid proteins VP1, VP2, and VP3 (Fig. (Fig.1).1). Large T-ag of SV40 strain 776 contains 708 amino acids and is a very multifunctional protein (Fig. (Fig.2).2). The large T-ag is an essential replication protein that is required for initiation of viral DNA synthesis and that also stimulates host cells to enter S phase and undergo DNA synthesis. Because of this ability to subvert cell cycle control, T-ag represents the major transforming protein of SV40. T-ag forms complexes with several cellular proteins; fundamental to T-ag effects on host cells is binding to cellular tumor suppressor proteins (91396116). These properties help explain SV40's potential as a tumor virus. However, it is important to point out that the oncogenic capacity of SV40 is an accidental side effect of the viral replication strategy; viral proteins (large and small T-ags) in lytically infected cells stimulate host cells into a state capable of supporting viral replication.
[Image: zcm0030420970001.gif]
FIG. 1.
Genetic map of SV40. The circular SV40 DNA genome is represented, with the unique EcoRI site shown at map unit 100/0. Nucleotide numbers based on reference strain SV40-776 begin and end at the origin (Ori) of viral DNA replication (map unit 0/5243). The ...

[Image: zcm0030420970002.gif]
FIG. 2.

Functional domains of SV40 large T-ag. Known T-ag functions are identified in boxes above and below the shaded bar, which represents the T-ag protein. The numbers given are amino acid residues based on reference strain SV40-776. The variable domain at ...
There is only one known serotype of SV40, but genetic strains exist and can be distinguished by nucleotide differences in the regulatory region (60) and in the variable domain at the extreme C terminus of T-ag, which is defined as the last 86 amino acids of the molecule (residues 622 to 708) (4758626381109110). Nucleotide differences in the T-ag C-terminal region, including polynucleotide insertions and deletions as well as single nucleotide changes, would change some encoded amino acids. These distinctions at the nucleotide and protein levels have conclusively established that SV40 sequences in human malignancies and other clinical samples are not the result of accidental laboratory contamination (Fig. (Fig.3,3, 4, and 5). However, future studies need to determine whether SV40 strains differ in pathogenic and/or oncogenic capacity. The classic example of DNA virus strains differing in oncogenic capacity is the human papillomavirus group; of the more than 75 types described, of which about 30 cause genital infections, only a few types are associated with the development of cervical carcinoma (68135). This identification of high-risk strains has led to the development of preventive interventions, such as the vaccine against human papillomavirus type 16 (54).

[Image: zcm0030420970003.gif]
FIG. 3.

SV40 large T-ag variable domains. (a) Schematic of large T-ag, showing the location of the variable domain. (b) Amino acid changes in the T-ag C-terminal variable domains of representative SV40 isolates and human primary brain tumor-associated sequences, ...
Laboratory-adapted monkey strains of SV40 typically contain two 72-bp enhancer elements (Fig. (Fig.44 and and5);5); these are designated “nonarchetypal” or complex regulatory structures (60). In contrast, SV40 isolates from human nonmalignant (Fig. (Fig.4)4) and malignant (Fig. (Fig.5)5) specimens usually (but not always) contain no duplications in the enhancer (“archetypal” structure).

[Image: zcm0030420970004.gif]
FIG. 4.
DNA sequence profiles of SV40 regulatory regions detected in human kidney transplant recipients. Ori, viral origin of DNA replication region, which spans nucleotides 5195 to 31; 21-bp repeats, GC-rich region between nucleotides 40 and 103; 72, 72-bp sequence ...

[Image: zcm0030420970005.gif]

FIG. 5.

Regulatory region of SV40. DNA sequence profiles of regulatory regions of SV40 isolates from monkeys and humans and of human tumor-associated DNAs are shown. The diagrams are labeled as described in the legend to Fig. Fig.4.4. Shown are laboratory-adapted ...

Although the function of the SV40 T-ag variable domain is not known, experimental data have suggested that it may be important in some aspect of the virus-host interaction. Embedded within the variable domain of large T-ag is a functional domain, which encompasses amino acids 682 to 708, defined as the host range/adenovirus helper function (hr/hf) domain (Fig. (Fig.2).2). A C-terminal fragment of T-ag can relieve the adenovirus replication block in monkey cells (23415190106) by an unknown mechanism. The hr function was identified because T-ag C-terminal deletion mutants exhibited different growth properties in monkey cell lines; the deletion mutants grew very poorly in CV-1 cells but grew well in BSC and Vero cells (2487118119). Viral DNA was replicated to near-wild-type levels in all three cell types (87108). Virions produced by the hr/hf mutants do not assemble properly, seemingly due to an inability to add VP1 to the 75S assembly intermediates (105).

The functional roles for another SV40 early protein, small T-ag, are more elusive. This protein is not essential for virus replication in tissue culture, and there is not a uniform requirement for it in SV40 transformation or tumor induction. However, studies indicate that SV40 small T-ag enhances large T-ag-mediated transformation (96) and is required for complete transformation of human cells in vitro (42). It inhibits cellular protein phosphatase 2A by complexing with the catalytic subunit and regulatory subunit of the enzyme. Small T-ag plays a role in the induction of telomerase in SV40-infected human mesothelial cells (36). Also, recent data indicate that small T-ag is required by large T-ag to upregulate Notch1 expression in SV40-infected and -transformed human mesothelial cells, as well as in SV40-positive human mesotheliomas (7).

Viral Replication Cycle and Effects on Host Cells

An appreciation of the replication cycle of SV40 is fundamental to understanding the oncogenic capacity of SV40 and its potential etiologic role in some human malignancies. The major histocompatibility class I molecules are the specific cell surface receptors for SV40 (48). This initial step in the viral cycle helps explain the broad tropism of the virus and its ability to infect and induce transformation in many types of cells and tissues. In addition, it provides an important distinction between SV40 and the other two polyomaviruses that are able to infect humans, JCV and BKV. JCV uses an N-linked glycoprotein and BKV uses a glycolipid as unique host cell receptors (3). These marked differences are believed to affect the nature of infections by these three viruses in tissues and individuals.

After infection of a cell, SV40 produces large and small T-ags early in the viral replication cycle. These antigens bind and block important tumor suppressor proteins, which include p53, pRb, p107, and p130/Rb2 (1135996) (Fig. (Fig.2).2). The functions of these intracellular proteins are centered in the control of the cell cycle. The tumor suppressor p53 is believed to sense DNA damage and either pauses the cell in late G1 for DNA repair or directs the cell to commit suicide through the apoptotic pathway (96116). SV40 T-ag binding sequesters p53, abolishing its function and allowing cells with genetic damage to survive and enter S phase, leading to an accumulation of T-ag-expressing cells with genomic mutations that may promote tumorigenic growth. pRb normally binds transcription factor E2F in early G1 of the cell cycle; T-ag causes unscheduled dissociation of pRb/E2F complexes, releasing E2F to activate expression of growth-stimulatory genes (96116). Therefore, SV40 infections in humans may interfere with several pathways related to cell cycle control and lead to development of malignancies.

Studies indicate that SV40 can replicate productively in human cells, including fetal tissues (101), newborn kidney cells (101), and different human tumor cell lines (83), although it grows poorly in human fibroblasts (84). Moreover, in vitro assays have shown that human cells can support replication of SV40, establishing that human proteins have the intrinsic ability to cooperate with SV40 T-ag to replicate SV40 DNA (6580127). Some human cell types undergo visible cell lysis in response to SV40, whereas others fail to exhibit cytopathic changes and produce low levels of virus (84). General conclusions from these early studies are that SV40 can replicate in human cells and that various human cell types display differences in susceptibility to infection by SV40. The basis for the differences is unknown, but T-ag functions are believed to be important (2769).
Recent studies have shown that primary human mesothelial cells respond to SV40 very differently from fibroblasts; the mesothelial cells are highly susceptible to SV40 infection and transformation. Most mesothelial cells were infected; few were killed; high levels of p53/T-ag complexes were present; Notch1, the hepatocyte growth factor receptor (Met), and insulin-like growth factor 1 were upregulated; and the tumor suppressor gene RASSF1A was inhibited (6153993). SV40-positive human mesotheliomas show similar changes. The rate of transformation of SV40-infected mesothelial cells was at least 1,000 times higher than that of human fibroblasts (6). These findings emphasize that different human cell types may display dramatically different virus-cell interactions during infection.

Transmission in Natural Infections

The recognized natural hosts for SV40 are species of Asian macaque monkeys, especially the rhesus macaque (Macacca mulatta). SV40, like the polyomaviruses JCV and BKV, establishes persistent infections, often in the kidneys of susceptible hosts (1359). An association of primary polyomavirus infection with mild respiratory tract disease, mild pyrexia, and transient cystitis has been reported (32), but the route of infection of these three viruses has not been firmly defined.

SV40 infections may become latent, and the level of virus present may be very low. Both viremia and viruria occur in infected animals, and virus shed in the urine is the probable means of transmission (297). SV40 infections in healthy monkeys appear to be asymptomatic (100), but SV40 causes widespread infections among monkeys that are immunocompromised due to simian immunodeficiency virus infection (475881); SV40 sequences and infectious virus were detected in brain, kidney, spleen, and peripheral blood mononuclear cells (PBMCs). These results demonstrate that SV40 can be an opportunistic pathogen in immunosuppressed hosts and that the virus may spread within the host by hematogenous routes.

Characteristics as a Tumor Virus

The oncogenic capacity of SV40 infections has been well established in laboratory animal models (91319111123). The latent period of tumor development in hamsters infected with SV40 ranges from 3 months to more than a year. The frequency of tumor development is usually over 90% in animals infected as newborns but is reduced in older animals. These data suggest that the age at the time of infection, the route of infection, and the duration of infection may be factors influencing the development of malignancies by SV40.

The neoplasias induced by SV40 in animal models include primary brain cancers, malignant mesotheliomas, bone tumors, and systemic lymphomas (1339123). Lymphomas are a common malignancy during SV40 infection. In hamsters inoculated intravenously with SV40, systemic lymphomas developed among 72% of the animals, compared to none in the control group (212930). The lymphomas were of B-cell origin (22). Following intravenous inoculation, about one-third of the animals developed more than one histologic type of neoplasm, with osteosarcomas being most common after lymphomas. Following intracardiac inoculation, malignant mesotheliomas and osteosarcomas developed in addition to lymphomas (19). An etiologic role of the virus in those cancers was supported because SV40 T-ag was expressed in all malignant cells, animals with tumors developed antibody against SV40 T-ag, and neutralization of SV40 with specific antibody before virus inoculation prevented cancer development (2930). Knowledge of these models prompted us, as well as other investigators, to consider the role of polyomavirus SV40 infections in some human malignancies.


HUMAN INFECTIONS BY SV40: OVERVIEW OF THE EVIDENCE
Although the prevalence of SV40 infections in humans is not known, studies conducted over the last three decades indicate that SV40 infections are occurring in child and adult populations today. These included individuals who received potentially SV40-contaminated vaccines, as well as in persons born after 1963 who could not have been exposed to those vaccines (511-141718252628404649556263666771-747678868889929495102104111115117120124125129130132133). In addition, 19% of newborn children and 15% of infants 3 to 6 months old at the time of receiving the oral contaminated polio vaccine were shown to excrete infectious SV40 in their stools for up to 5 weeks after vaccination (75). It is important to point out that the incidence of SV40 infections linked to those vaccines is not known.

SV40 seroprevalence rates in the general populations of the United States and other countries have ranged from 2 to 20% (137895). However, differences in the methodology and low sensitivity of the assays used in some studies make it difficult to ascertain the actual prevalence of SV40 infections. A report by Shah et al. (99) found that 18% of adult kidney transplant patients had specific neutralizing antibody to SV40. Another study among adult patients showed the presence of SV40 neutralizing antibodies in 16% of human immunodeficiency virus-infected patients and 11% of individuals not infected with human immunodeficiency virus (49). Among hospitalized children, the overall prevalence of specific SV40 serum neutralizing antibodies was 6% (12); the SV40 seropositivity among children increased with age (P = 0.01) and was significantly associated with kidney transplantation (P < 0.001) (Table (Table1).1). Recently, a study of the prevalence of SV40 infections showed rates of 9% in Hungary and 4% in the Czech Republic (14). Females had a higher rate of SV40 antibodies than males, reaching 16% in Hungary and 8% in the Czech Republic in certain age groups. SV40 infections were found in similar proportions in both countries among persons not exposed to potentially contaminated polio vaccines and in subjects vaccinated in the era of SV40-free vaccines. Minor et al. (78) recently analyzed over 2,000 sera from the United Kingdom and found an SV40 seroprevalence rate of just under 5%. Most of the neutralizing titers were low, and there was no apparent relationship between antibody positivity and polio vaccine usage. These data suggest that SV40 is being transmitted in the human population today, probably at a relatively low prevalence rate. However, conclusions about seroprevalence rates should be viewed with caution, as very little is known about the human immune response to SV40 infections.
[Image: ?report=thumb]
TABLE 1.

SV40 seropositivity of hospitalized children in Houston, Tex.a
Although the mode of transmission of SV40 among humans is unknown, we speculate that different routes may be involved. Studies with laboratory animals indicate that maternal-infant transmission is one possible route of SV40 spread (91). This may represent a pathway for SV40 infections in humans (of unknown frequency), as there are reports of the detection and expression of SV40 T-ag and the presence of viral DNA in cases of primary brain cancers in infants and young children (57172117129133). Also, evidence indicates that zoonotic transmission of SV40 should be a consideration in certain populations. Indeed, laboratory workers in contact with SV40-infected monkeys and/or tissues from those animals had a prevalence of antibodies to SV40 in the range of 41 to 55%, suggesting an increased risk for viral infection among this group of workers (43134).
Molecular studies of adult patients with renal disease and recipients of kidney transplants found that SV40 cytopathic effects developed in CV-1 cells cocultured with urinary cells or PBMCs from those patients (6667). SV40 sequences were detected by PCR in kidney biopsies from 56% of patients with focal segmental glomerulosclerosis. SV40 DNA was localized to renal tubular epithelial cell nuclei in renal biopsies of patients with focal segmental glomerulosclerosis as determined by in situ hybridization. In addition, studies showed that SV40 DNA sequences from the viral regulatory region were detected and identified in the allografts of immunocompromised pediatric renal transplant recipients (Fig. (Fig.4)4) and in the native kidney of a young adult lung transplant patient with polyomavirus nephropathy (111277). Different studies have detected SV40 DNA sequences in PBMCs from various patient populations (2631667273132). These results demonstrate the nephrotropic and lymphotropic properties of SV40 and indicate that the kidney can serve as a reservoir for the virus in humans. It appears that patients with acquired and/or iatrogenic immunosuppression are a population at risk for SV40. However, the frequency, natural history, and morbidity of the virus in this increasing patient population are unclear.

Large prospective studies using sensitive and specific reagents for SV40 are needed to determine the prevalence of viral infections in the general population and to define groups of individuals at elevated risk for this emerging pathogen. Similarly important is the need for prospective longitudinal studies that address the morbidity and related mortality of these infections. The use of serologic tests alone may not be the most reliable way to conduct these studies. An enzyme immunoassay method for detection of SV40 antibodies in humans recognizes cross-reactivity between SV40, BKV, and JCV, complicating interpretation of assay results (126). Similar limitations have been found in serologic methods for identification of human infection with herpes B virus (Cercopithecine herpesvirus 1), which is known also to naturally infect rhesus macaques (M. mulatta) (45). Because infection with B virus in humans results in fatal encephalomyelitis or severe neurologic impairment, rapid and conclusive diagnosis is critical in order to control sequelae by this viral pathogen. Serologic assays (including enzyme immunoassay) for B-virus infection in humans are limited by low sensitivity and specificity (45). Currently, cell culture for the three polyomaviruses known to infect humans (JCV, BKV, and SV40) is rarely helpful in establishing diagnosis of infection because of slow viral growth and the requirement for specialized cell lines (5256). Serologic assays may be useful for retrospective epidemiological analysis, but they are of minimal use for diagnosis or therapeutic decisions because most overt polyomavirus infections are believed to result from reactivation of latent infections (5256). Therefore, the use of modern molecular biology assays is an excellent and preferred alternative for the analysis of SV40 infections in the human population (123). In addition, these sensitive and specific techniques are able to provide insights into the possible infectious etiology of human malignancies (3779123).


ROLE OF SV40 IN HUMAN CANCER
Experimental Approaches
During the last decade, many studies have shown the presence of SV40 large T-ag DNA or other viral markers in primary human brain and bone cancers, malignant mesotheliomas, and NHL (Fig. (Fig.6).6). Sequence analyses (Fig. (Fig.33 and and5)5) and detection of T-ag protein (Fig. (Fig.7)7) ruled out laboratory contamination of tumor samples. Importantly, infectious SV40 was isolated from a primary brain cancer of a 4-year-old child (62). An important consideration when evaluating the molecular biology data is the sensitivity of methods used to detect SV40 in human tumor samples. Early studies (before 1992) identified SV40-positive neoplasms by using indirect immunofluorescence for viral proteins or DNA hybridization techniques (5574130), whereas studies after 1992 generally used PCR-based assays.

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FIG. 6.
Detection of SV40 T-ag DNA in NHLs. (A) PCR-amplified polyomavirus sequences after agarose gel electrophoresis and staining with ethidium bromide (upper panel) and after Southern blotting with oligonucleotide probes specific for individual polyomaviruses ...

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FIG. 7.

(A) Immunohistochemical detection of SV40 T-ag in a diffuse large B-cell NHL. (B) Negative control specimen (a reactive lymph node). Specimens were stained by using a monoclonal antibody, PAb416. Note the strong nuclear staining of the majority of lymphoma ...

During the last three decades more than 60 original studies have reported the detection of SV40 in primary brain and bone cancers, malignant mesothelioma, and NHL, whereas a few studies have described an absence of SV40 in those malignancies (163334444870113). However, the small numbers of samples tested, the histologic types of malignancies examined, and the laboratory methodologies employed in some cases limit the significance of the results in those studies reported to be negative. Indeed, several steps need to be considered when performing molecular studies of human specimens (15061107). First, the extraction step of nucleic acids determines whether tissues yield adequate and suitable DNA or RNA for analysis. Unfortunately, with formalin-fixed and paraffin-embedded specimens, degradation of nucleic acids and proteins is a common problem, and the quality of recovered DNA may be poor. If only small amounts of paraffin-embedded tissues are available, the yield of nucleic acids may be inadequate for analysis. Primers directed to a human cellular gene should be used to establish the suitability of a sample for PCR analysis. Because of the sensitivity of PCR-based assays, it is important to rigorously guard against laboratory contamination of samples and controls during processing or testing. Tissue processing and PCR assay setup should be performed in different facilities, from which positive controls (i.e., plasmids) are excluded. Negative tissue controls, extracted and analyzed in parallel, should be included in each experiment to monitor for reagent contamination. The selection of primers and PCR conditions greatly influences the sensitivity and reliability of the assay. Another factor is that tumor specimens usually contain mixtures of normal and malignant cells, in varying proportions. Variations in one or more of these important parameters may explain, at least in part, the ranges in positivity observed among some positive studies and the results obtained in some negative studies.

Summary and Meta-Analysis of Controlled Studies

Table Table22 provides a timeline for landmark discoveries associating the polyomavirus SV40 and human malignancies. Although numerous studies have detected SV40 in human primary brain and bone cancers, malignant mesothelioma, and NHL, the small sample sizes and the lack of a control group in some studies made it difficult to make conclusions about the extent to which SV40 may be associated with those human cancers. For this reason, we conducted a meta-analysis of controlled studies (122), an approach which can provide a more balanced and less biased estimate of the evidence than individual studies (57). For inclusion in the meta-analysis, reports had to meet the following criteria: studies were conducted among patients with primary malignancies, the investigation of SV40 was performed on primary cancer specimens and not on cultured cells, the analysis included a control group, and the same laboratory technique was used for both case and control samples. These criteria were established because the use of appropriate controls is crucial in the proper analysis of tissue for viral DNA, especially considering the sensitivity of PCR techniques (38). Thirty-five independent studies met these inclusion criteria. In total, data from 1,793 patients with primary malignancies were evaluated to determine whether SV40 is significantly associated with primary brain cancer, malignant mesothelioma, bone cancer, and NHL.

[Image: ?report=thumb]

TABLE 2.

Timeline for discoveries associating SV40 and human malignancies

Thirteen studies fulfilled the criteria for the investigation of primary brain cancers (Table (Table3).3). The combined odds ratio (OR) of the studies used in the analysis was 3.9 (95% confidence interval [CI], 2.6 to 5.8). This effect was based on specimens from a total of 1,143 patients, of which 661 were primary brain cancer samples and 482 were control specimens. A modifier detected was the type of sample analyzed (paraffin embedded versus frozen). The adjusted OR was 3.8 (95% CI, 2.6 to 5.7). For malignant mesothelioma, 15 studies fulfilled the criteria; the combined OR of analysis was 16.8 (95% CI, 10.3 to 27.5) and was based on 528 patients with malignant mesothelioma and 468 controls (Table (Table4).4). Modifiers detected were the type of control tissue and the method of detection of SV40. The adjusted OR was 15.1 (95% CI, 9.2 to 25.0). The combined OR of the analysis of bone cancers and SV40 was 24.5 (95% CI, 6.8 to 87.9) and was based on 303 patients with bone tumors and 121 controls from four reports (122). The OR for NHL was 5.4 (95% CI, 3.1 to 9.3) and represented 301 cases and 578 controls included in three studies (Table (Table5).5). Because there were only three studies that fulfilled the inclusion criteria, further examination of modifying variables was not possible for NHL.

[Image: ?report=thumb]

TABLE 3.

SV40 in primary brain tumorsa
[Image: ?report=thumb]
TABLE 4.

SV40 in malignant mesotheliomasa
[Image: ?report=thumb]
TABLE 5.

SV40 in NHLsa
This analysis of published reports found a significant excess risk of SV40 associated with human primary brain cancers, malignant mesotheliomas, bone cancers, and NHL compared to control samples. Therefore, the major types of human malignancies associated with SV40 are the same as those induced by SV40 in animal models. Although the proportion of human cancers containing SV40 varied from study to study, viral prevalence was always greater among primary tumors than among control tissues. Importantly, analysis of data indicated that SV40 may be etiologically meaningful in the development of a specific subset of human cancers. Multiple studies have shown the expression of SV40 mRNA and/or T-ag in cancer cells, the integration of SV40 sequences in some cancers, and SV40 T-ag protein complexed with p53 and pRb in some tumor specimens (11013395076122). These findings are compatible with current understanding of how SV40 T-ag mediates oncogenesis. Moreover, microdissection of human malignant mesothelioma samples followed by PCR detected SV40 T-ag DNA only in cancer cells and not in adjacent nonmalignant cells (139104). These results from different experimental studies support the conclusion of the Institute of Medicine (111) that “the biological evidence is of moderate strength that SV40 exposure could lead to cancer in humans under natural conditions.”


FUTURE DIRECTIONS AND CONCLUSIONS
Mounting evidence indicates that SV40 is a human pathogen, and current molecular biology, pathology, and clinical data, taken together, show that SV40 is significantly associated with and may be functionally important in the development of some human malignancies. Now, prospective studies are needed to determine the prevalence of SV40 infections in different human populations and to assess how the virus is transmitted from person to person. Indeed, the Institute of Medicine recognized that this gap in our understanding of the pathogenesis of SV40 in humans is important and recommended “targeted biological research” of SV40 in humans, including “further study of the transmissibility of SV40 in humans” (111).

Considering that molecular biology approaches provide sensitive and specific approaches to analyze infectious diseases and malignancies with a possible infectious etiology, studies using these modern methods should be used to assess the distribution of SV40 infections and morbidity in humans today.

Although in vitro studies have established that SV40 disrupts critical cell cycle control pathways, it remains unknown whether these perturbations are sufficient for the virus to induce the development of malignancies in humans. Therefore, animal models that reproduce key features of SV40 infection and disease in humans are needed. Such models could provide precise evidence of the causal role of a particular pathway in SV40 pathogenesis in target tissues, allow further characterization of the molecular mechanisms of oncogenesis, and provide a preclinical system to test therapeutic interventions for these significant and increasingly common diseases.


ACKNOWLEDGMENTS
This work was supported in part by grant R21 CA96951 from the National Cancer Institute. Regis A. Vilchez is the recipient of the 2001 Junior Faculty Development Award from GlaxoSmithKline and the 2002 Translational Research Award from the Leukemia and Lymphoma Society.


Looks more like conspiracy fact
#7
Thank you for all that information @"Armonica_Templar".   minusculethumbsup2 

Big Pharma and the Elite have been working on the depopulation agenda a long time it appears.
Doesn't surprise me at all. tinyok
#8
(10-17-2017, 05:52 PM)Wallfire Wrote: Well if its true, it could explain why so many people in there 40s upwards are getting the big C. I just got my anti flu injection today hope its free of any additives tinybighuh

@"Wallfire", you might want to read this.   :smallundecided: 

BOMBSHELL: Flu shots scientifically proven to weaken immune response in subsequent years… researchers stunned Tuesday, October 17, 2017 by: Mike Adams
#9
Every story has at least two sides, always good to know at least some of them  minusculebiggrin

If You Know Anyone Afraid of the Flu Shot, Show Them This!

Posted on October 20, 2016 by Stephen Propatier
Internet memes are constant reminders of how unstructured information sharing is. I see memes through the prism of scientific skepticism and critical thinking and the most frustrating aspect is how they can be used to disseminate dangerous ideology and disinformation. There is no end to the structured disinfo out there—from creationism to anti-vaccine doggerel—everywhere on the Internet. Fear mongering has become an art form in promoting the agendas of ideologues, often using reasonable-sounding but myopic anti-science propaganda. This is especially dangerous during flu season.

Fear mongering plays on our fallible human brain, our innate fear of the unknown,with a dash of the precautionary principle to structure a scare tactic. The anti-science themes and memes are artfully packaged to frame the conversation to their agenda. Facebook popularity makes it ground zero for such nonsense. Given the fact that the Influenza season approaches there is little surprise that the anti-vaccine disinformation machine throws its annual fear pamphlet out on Facebook for all to pass around. Fear mongering about the flu vaccine with exaggerated or false claims. Dressed up nicely with click bait headlines, scary words, and ominous claims of experts and research. Lets turn our skeptical eye to a viral Facebook article that personifies false anti-vaccine arguments.
A salacious listicle from LoveThisPic.com, titled “If You Know Anyone Thinking Of Getting A Flu Shot Give Them This!” [sic] has recently been circulating on Facebook. This is complete and utter bunk, anti-vax propaganda, written with just the right amount of science-y sounding words and tired, disproved vaccine claims to give the average person pause. Since a lay person would most likely Google the claims, they will see an avalanche of anti-vax sites duplicating those false ideas. It raises the likelihood that an honestly concerned person will get inaccurate confirmation of those fears. Let’s pull apart this tent of lies and give you the real answers that the anti-vaccine crowd doesn’t want you to know.
[img=0x0]https://i2.wp.com/upload.wikimedia.org/wikipedia/commons/thumb/5/53/Fight_flu_early_with_vaccine_141020-M-IY869-017.jpg/640px-Fight_flu_early_with_vaccine_141020-M-IY869-017.jpg?resize=640%2C480&ssl=1[/img]Single-dose flu vaccine. Via Wikimedia
So here are 11 lies about the flu vaccine, revisited:
1. The flu shot makes you sickMostly wrong. Although live attenuated influenza vaccines (LAIVs), such as flu mist, could possibly give an active but very weak case of the flu, it is almost unheard of. That kind of nasal LAIV is not available this year; all forms of vaccine are either recombinant proteins or a complete killed virus. Although some people feel slightly ill after taking the vaccine, this is just the immune system reacting to the vaccine and making antibodies to destroy the actual disease. It has none of the cell-damaging effects of the actual disease.
2. Flu vaccines contain other dangerous ingredients such as mercury—Wrong! First, it’s important to note that almost no flu vaccines even contain thimerosal, and children are not given thimerosal in the vaccines they receive. The only US vaccine left with thimerosal is Fluvirin, from Noventis, which contains 0.0000001 grams mercury per dose. (You inhale more mercury from air pollution than you get from a dose of Fluvirin.) It is only given to adults. Neither single-dose shots nor nasal spray versions of the flu vaccine contain any mercury compounds. The multi-dose flu shot does contain a preservative called thimerosal, which breaks down into 49% ethylmercury and is used to prevent bacterial contamination of the vaccine container. It’s important to understand the difference between two different compounds that contain mercury: ethylmercury and methylmercury. They are totally different materials.
Methylmercury is formed in the environment when mercury metal is present. If this material is found in the body, it is usually the result of eating some types of fish or other food. High amounts of methylmercury can harm the nervous system. In the United States, federal guidelines keep as much methylmercury as possible out of the environment and food, but over a lifetime, everyone is exposed to some methylmercury.
Ethylmercury is formed when the body breaks down thimerosal. The body removes ethylmercury from the blood quickly. Low-level ethylmercury exposures from vaccines are very different from long-term methylmercury exposures, such as from tainted foods, because ethylmercury does not stay in the body. Again, you consume more mercury from air pollution than you could from the only vaccine that has thimerosal.
3. The flu shot can cause Alzheimer’s disease—A bald-faced lie. All the best evidence at this stage is that Alzheimer’s is a genetic disease. There is no credible evidence for this claim at all.
4. The people pushing flu vaccines are making billions of dollars a year—This is wrong in so many ways it’s beyond wrong. Even if it were true, so what? If vaccines are profitable it doesn’t automatically mean they’re useless and deadly. Many products make multiple billions of dollars and are totally safe. Companies don’t just recommend flu vaccination—medical professionals do. There are plenty of medically literate vaccine supporters who don’t get a dime. I, for example, support vaccines and I have written extensively in favor of vaccines. I am an orthopedist with no financial interest in vaccines in any way. We don’t even have them available to give to our patients, any more than I have antibiotics.
But let’s ignore the fallacy of the main statement and put this in context of the worldwide sales of all pharmaceutical products in 2013—nearly $1 trillion worth of sales. Various flu vaccines make up less than 0.3% of worldwide sales of “Big Pharma,” so from a strategic point of view, they’re not that interesting an incentive. Just for context, cholesterol-lowering drugs, e.g. statins, made more than $33 billion two years ago. If I were a Big Pharma executive, I’d be telling my R&D and marketing divisions to invest in new statins, because the potential return on investment could be 10x higher. And that’s exactly what they do. In 2013, the top-selling drugs were daily medications, such as for diabetes, pain, inflammation, blood pressure, cholesterol, and depression. A single-dose-per-year medicine doesn’t make much difference to the bottom line of drug companies.
Let’s examine those sales in context of the three biggest companies in this particular vaccine sector:

Quote:Sanofi Pasteur: Total sales $41.6 billion. Flu vaccine sales $1.3 billion. In other words, flu vaccine makes up around 3% of their sales
Glaxo SmithKline: Total sales $32.3 billion. Flu vaccine sales $420 million, or 1.3% of their total sales.
Novartis: Total sales $57.9 billion. Flu vaccine sales $215 million, or 0.4% of their sales.

Note: the remaining $1.1 billion in flu vaccine sales is spread over 15 other manufacturers, none of whom have a major market share. And much of these sales are to public organizations (which cap prices) and to developing nations.
If Big Pharma were run solely for profit over all other considerations, then they would stop making vaccines. (Indeed, some have.) It is far more profitable to treat the disease than it is to prevent it, which, ironically, is a common half-baked claim about modern medicine by the anti-science ideologues. If pharmaceutical companies stopped selling flu vaccines, it is estimated that there would be an extra preventable 78,000 hospitalizations in the USA. In addition, the estimated annual deaths from flu would probably be 6,000 to 100,000 individuals. Setting aside the costs of lost productivity and deaths from the flu (tens of billions of dollars), hospitalizations alone would cost around $4,000 per individual, or a total of nearly $300 million. Furthermore, in a full-blown flu outbreak, millions of individuals would visit their physicians and emergency rooms, adding another $1 billion or more in health care costs. And that’s just the USA. These costs would probably be three to five times greater if we looked at the whole planet. And Big Pharma would capture about 30-40% of those healthcare costs, for consumable supplies, drugs, treatments for secondary infections, and other products. And these products have a much higher gross profit than vaccines.
In other words, if we assume that pharmaceutical company decisions are strictly driven by cold blooded profit, it might make more sense to under produce enough vaccine or stop selling the flu vaccine altogether, and sell supplies to the hospitals and physician offices. But that isn’t the case, obviously. It would also be extremely short-sighted and dangerous.
5. Lack of real evidence that young children and the elderly even benefit from the flu shots—This is a very harmful lie. The most vulnerable populations are the elderly and children, along with people with compromised immune systems. They have the highest risk of vaccine failure because their immune system is weak or underdeveloped. It’s not because the vaccine is ineffective; rather, it is the insufficient response of their weak or underdeveloped immune system. The reason why everyone needs to be immunized is to protect them. They are the weak and need to be protected with herd immunity. That’s where the vaccine protects them, by keeping it away from the little babies and the very old. By avoiding the vaccine, you’re dooming them to rely on their own defenses. Even if they do not receive the flu vaccine, the benefits for children and the elderly are without question.
6. Vaccines make you susceptible to other diseases—The reverse of this is actually true. Vaccination empowers your immune system, while being unvaccinated is more draining and dangerous. Catching the flu will weaken your immune system, and while you’re sick it’s easier to become ill from other bugs. But more importantly, pneumonia is among the most common complications to occur as a result of a flu infection. Getting the flu shot reduces your risk of pneumonia, a leading cause of death among those who die from influenza complications.
7. They cause vascular disorders—There is no evidence that the flu vaccine causes vascular disorders. Meanwhile, the vaccine has been shown in multiple studies to reduce individuals’ risk of heart attacks, stroke, and other cardiovascular events.
8. They are risky for children under the age of 1—This is an utter falsehood, based on the wrong claim that a young child’s blood-brain barrier is underdeveloped. There is no evidence that flu vaccines can hurt children’s development or that children’s neuro-vascular structures are affected by flu vaccines. A child’s blood-brain barrier is formed in utero and is functional from birth in regulating what can and cannot pass into the brain. Researchers at Stanford University and the University of California, San Francisco discovered in 2010 that pericytes, required for blood-brain barrier development, are present in the fetal brain. The physiology of the blood-brain barrier and how it functions at that level of development make it highly implausible that any vaccine components could penetrate the barrier.
9. Increased risk of narcolepsy—This is one of the few myths that is rooted in a small amount of fact, though it’s often misrepresented or blown out of proportion. Narcolepsy is a neurological disorder in which the brain in unable to regulate sleep-wake cycles. Several studies, first in Finland and then in other European countries, found and confirmed a link between narcolepsy and the 2009 H1N1 flu vaccine called Pandemrix, manufactured by GlaxoSmithKline Europe and used in several European countries (but not in the US or Canada). It was not used before 2009 or since the 2009–10 season, and no links to narcolepsy have been found for US-manufactured H1N1 or seasonal flu vaccines. The CDC sponsored an international study on the link between the 2009 H1N1 flu vaccines and narcolepsy,  it was published in 2014 and doesn’t support any danger .
10. Weakens immune responses—Influenza vaccines actually strengthen the immune system, activating a response that leads to the production of specific antibodies against the disease the vaccine is designed to protect against. In fact everyone should actually think about this as an immune system “workout.” Training the muscle to fight a future invader. You might get a little sore but no damage is done and in the end you have a stronger muscle not a weaker one.
11. Serious neurological disorders—This claim is also totally, completely wrong. Anti-vax propagandists love to fear-monger about Guillain-Barré syndrome (GBS). Guillain-Barré is associated with influenza, the disease, but not the vaccine, and GBS is rare. Medical events occur regardless of vaccination, and background rates are used to assess vaccine safety by comparing the expected rate of disease or death to the actual or observed rate in any given timeframe. The background rate for GBS in the U.S. is about 80 to 160 cases of GBS each week, independent of vaccination. According to our friends at Science-Based Medicine, “Guillain-Barré syndrome affects 1 to 4 of every 100,000 people around the world every year, and the increased risk from vaccines is currently estimated at no more than 1 in a million.” And that was in spite of other problems in the shaky data used to come to that estimate.
So, 11 oft-repeated falsehoods about getting the influenza vaccine. It requires some digging to get at the truth, but there’s a lot of evidence against each claim. So here’s the truth, no digging. Be sure to pass it around Facebook as generously as the misinformation is being shared. I’m getting my influenza vaccine this week; make sure you get yours
!
#10
I put up a thread a few months ago about a series on the different kinds of vaccines.  You had to sign up to watch them. You got one show per day in your e-mail for 9 days, and had 24 hrs. to watch it.
I can't share it here, but I hope my thread got people to sign up to watch.  It had some of the most "in the know" people available who were speaking out about the dangers of several vaccines, and the flu vaccine was one included.

People can do as they wish.

There will always be those who think it's all fear mongering, but then, there will be those who pay attention to the warnings and take the advice offered. It's to those willing to listen that I put this information out.

And, for what it's worth, those reports you see from the lab researchers on medicines have been tainted by Big Pharma goons telling the researchers what they CAN, or CAN'T put in the report.  This was also covered in the series I watched by people in the field.
#11
Its always good to get as much info as possible, thats why people like you (MW) and sites like this are so important   minusculebeercheers


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