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retroviruses are back in news

anciendaze

Senior Member
Messages
1,841
For anyone who still believes the only retroviruses infecting humans are HIV and HTLV, I would like to reference this Berkeley announcement and this published paper. This follows a relatively unnoticed publication last year showing bovine leukemia virus (BLV) could be found in humans. Since antibodies to BLV are found in essentially all milk tankers, and in people who drink unpasteurized milk, the reason for saying the virus was not found in humans, based on old studies with very low sensitivity, is hard to square with virtually all work on retroviruses in non-human animals.

If the virus is passed from mother to infant prior to weaning, and the effects do not appear until after sexual maturity, we have to expect the rate of replication to be inversely proportional to the time between weaning and sexual maturity, which is unusually long in humans. A virus which replicates faster would often kill infected individuals before they could pass it on, likely becoming extinct.

We don't know that the virus is the cause of this human disease, though similar viruses cause virtually all mammary tumors in some other mammals. Also, patients on ARVs are known to have lower rates of breast cancer. There is a possibility the association takes place after onset. This still leaves the question of markers associated with both infection and onset which might lead to early detection --- when the problem is easy to treat. Early detection has long been a research goal.

The size of the reported increase in risk is larger than most other known factors. The effects of this disease are undeniably serious, and the number of cases is substantial. So why has this possibility, and the chance to reduce incidence of breast cancer, met with such strong opposition over a period of many years?

In cattle the disease most obviously associated with BLV is bovine leukosis, but many cattle tolerate infection without displaying symptoms. Leukocytes are the cells most affected, and many diseases associated with impaired immune response could be the result of retroviral infection of leukocytes.
 
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barbc56

Senior Member
Messages
3,657
The virus could have come through the consumption of unpasteurized milk or undercooked meat, or it could have been transmitted by other humans
.

Interesting study. Does the above mean that pasteurized milk would not have the virus?

Barb
 

alkt

Senior Member
Messages
339
Location
uk
more scary health news but they mention possible future prevention wouldn't they need to know how blv gets into human breast tissue in the first place.
 

anciendaze

Senior Member
Messages
1,841
more scary health news but they mention possible future prevention wouldn't they need to know how blv gets into human breast tissue in the first place.
The virus is known to infect leukocytes, and leukocytes do enter breast tissue. They are even passed to nursing infants via milk. There is no particular argument about whether or not the virus can infect human leukocytes in vitro.

If you compare female human breasts with other primate breasts (as Hugh Hefner has done at great length) you will note that humans have unusually large breasts. A very plausible suggestion is that this means greater milk production, which would tally with increased dependence of human infants on suckling for nutrition. I can't think of another mammal that goes so long before weaning.

The biological problem with this is that increase in the amount of unusual fat and protein in breast tissue, plus the length of time it is present, is likely to provoke an autoimmune response. My suggestion is that retroviral infection has played a role in this evolutionary change by producing localized immune suppression in these tissues.

Even if it is hard to trace this directly to the infection there is another aspect of retroviral infections which comes into play: active retroviral infections do a very good job of stimulating transcription of HERVs. This could well be a kind of defense by the local resident ERVs to competition from outsiders. These defective sequences not only compete for cellular resources, they also recombine with sequences transcribed from inserted provirus. The result is that the invading sequence is less successful in replication, and more likely to end up resembling other HERVs. When this process slows replication to the point that infected infants can survive to produce offspring the new virus has joined the club of existing endogenous viruses.

As evidence that this really takes place, I point out the observed fact that the last parts of ERVs to be corrupted are the LTRs. These are simple repetitive sequences which contain receptor elements that control transcription. No matter how badly corrupted the actual genes are, ERV sequences will continue to be transcribed as long as those LTRs persist.

While the classic retroviral replication cycle can be disrupted by mutational defects in any gene, some genes can survive and produce functional biochemicals even if the cycle of replication fails. The sequences which interest me most are those which code for immunosuppressive domains in viral envelopes.

One complicating factor in research on retroviruses and breast cancer has been the large number of copies of HERV-K111 which went a long time without being located. These genes hidden in centromeres have been thoroughly sliced and diced by evolutionarily recent changes. This meant that infection by BLV triggered transcription of defective sequences derived from beta retroviruses resembling MMTV. This is not very specific, HIV also triggers transcription of these sequences. HIV is a lentivirus, while BLV is a delta retrovirus, and MMTV is a beta retrovirus.

The result is that narrow concentration on specific sequences which "breed true" will become lost in a "smoke screen". The virus causing this "smoke" isn't trying to frustrate researchers, it is busy hiding from immune response. Because of the slow replication needed to avoid killing hosts quickly the sequences researchers need to look for will be rare. Those immunosuppressive domains in envelope genes from defective provirus will still function to provide limited immunosuppression in tissues where they are active.

Host species can benefit from this when local immunosuppression boosts fertility and reproductive success, even if the end result for individuals is an agonizing death after reproductive age. Infected individuals who live long enough to produce offspring pass on both their genes and the retrovirus. If the sum total of these processes aids differential reproductive success, they will come to dominate the host population.
 
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anciendaze

Senior Member
Messages
1,841
A few countries have eliminated BLV from their dairy herds, but the U.S. is not one of them. It is still far too early to expect epidemiological results about an infection which persists for decades before clear signs of disease appear.
 

alkt

Senior Member
Messages
339
Location
uk
The virus is known to infect leukocytes, and leukocytes do enter breast tissue. They are even passed to nursing infants via milk. There is no particular argument about whether or not the virus can infect human leukocytes in vitro.

If you compare female human breasts with other primate breasts (as Hugh Hefner has done at great length) you will note that humans have unusually large breasts. A very plausible suggestion is that this means greater milk production, which would tally with increased dependence of human infants on suckling for nutrition. I can't think of another mammal that goes so long before weaning.

The biological problem with this is that increase in the amount of unusual fat and protein in breast tissue, plus the length of time it is present, is likely to provoke an autoimmune response. My suggestion is that retroviral infection has played a role in this evolutionary change by producing localized immune suppression in these tissues.

Even if it is hard to trace this directly to the infection there is another aspect of retroviral infections which comes into play: active retroviral infections do a very good job of stimulating transcription of HERVs. This could well be a kind of defense by the local resident ERVs to competition from outsiders. These defective sequences not only compete for cellular resources, they also recombine with sequences transcribed from inserted provirus. The result is that the invading sequence is less successful in replication, and more likely to end up resembling other HERVs. When this process slows replication to the point that infected infants can survive to produce offspring the new virus has joined the club of existing endogenous viruses.

As evidence that this really takes place, I point out the observed fact that the last parts of ERVs to be corrupted are the LTRs. These are simple repetitive sequences which contain receptor elements that control transcription. No matter how badly corrupted the actual genes are, ERV sequences will continue to be transcribed as long as those LTRs persist.

While the classic retroviral replication cycle can be disrupted by mutational defects in any gene, some genes can survive and produce functional biochemicals even if the cycle of replication fails. The sequences which interest me most are those which code for immunosuppressive domains in viral envelopes.

One complicating factor in research on retroviruses and breast cancer has been the large number of copies of HERV-K111 which went a long time without being located. These genes hidden in centromeres have been thoroughly sliced and diced by evolutionarily recent changes. This meant that infection by BLV triggered transcription of defective sequences derived from beta retroviruses resembling MMTV. This is not very specific, HIV also triggers transcription of these sequences. HIV is a lentivirus, while BLV is a delta retrovirus, and MMTV is a beta retrovirus.

The result is that narrow concentration on specific sequences which "breed true" will become lost in a "smoke screen". The virus causing this "smoke" isn't trying to frustrate researchers, it is busy hiding from immune response. Because of the slow replication needed to avoid killing hosts quickly the sequences researchers need to look for will be rare. Those immunosuppressive domains in envelope genes from defective provirus will still function to provide limited immunosuppression in tissues where they are active.

Host species can benefit from this when local immunosuppression boosts fertility and reproductive success, even if the end result for individuals is an agonizing death after reproductive age. Infected individuals who live long enough to produce offspring pass on both their genes and the retrovirus. If the sum total of these processes aids differential reproductive success, they will come to dominate the host population.
thank you for such an in depth and for me educational post.