ACV inhibits HIV in herpesvirus-infected cells

[Daffodil]

Hello. This might explain why, even if we are infected with a retrovirus, many of us respond to anti-herpes drugs. Apparently, acycolovir inhibis HIV also, in cells that are already infected with herpes viruses:

http://www.sciencedaily.com/releases/2008/09/080910133651.htm

 

[Enid]

Good find Daffodil - many thanks - is there more to the herpes virus in all it's forms

 

[anciendaze]

This is also true of other drugs in the same family. It was one clue which started me on a search for drugs which might accidentally treat viral and retroviral infections. Simply because minocycline (or doxycycline) is labeled an antibiotic does not mean it will have no effect on viral infections. My list grew quite long before the topic became unwieldy, and I had to back off from my original goal. More recent results along the same lines include the discovery that fluoxetine (Prozac) strongly inhibits a common enterovirus in vitro. A surprising number of drugs often given to patients with mysterious complaints may actually be treating unidentified viral infections.

Enid, I'm afraid I don't follow your question. Could you restate it?

 

[Enid]

ancendaze - just that some in the family of herpes viruses have appeared suspect before (as playing a role) so interesting to see anything on the topic. Acyclovir in particular though I know the findings relate more to HIV here. Interesting to follow your thoughts on the "accidental" too.

 

[anciendaze]

My thoughts on the whole group of human herpes viruses are that they appear to be commonly reactivated by this disease, though not always the same virus. Essentially every human herpes virus from HHV-1 (HSV-1) to HHV-8 is involved. Many of these are practically endemic in humans, but commonly remain latent for most of a lifetime. This points to an acquired defect in the mechanisms which hold viral infections latent. Most people who are seriously ill with this disease have multiple active (but not acute) viral infections. Many of these are HHVs, like EBV, CMV, VZV, but not all. Parvoviruses, adenoassociated viruses and bocaviruses are examples of other DNA viruses you may see. Enteroviruses are examples of RNA viruses which sometimes cause these symptoms. If all these are not separate and unrelated diseases there appears to be a fundamental acquired immune defect which (usually) remains limited, unlike AIDS. Limited immunosuppression is the clue which makes me consider retroviruses seriously.

I feel the need at this point for a disclaimer, I do not believe the course of the infection is the same in all people. I am now convinced that over 90% of those infected generally remain asymptomatic, except in cases where some other insult damages immune response. In those exceptions, there is always some confounding factor which can be blamed. Our political problem is that 90+% of the population is not especially vulnerable, most of the time. What happens when they grow old is another matter entirely. The similarity between our symptoms and those of aging people convinces me many more people are affected at some stage in life. Connect the dots, and political will should follow.

 

[natasa778]

My thoughts on the whole group of human herpes viruses are that they appear to be commonly reactivated by this disease, though not always the same virus. Essentially every human herpes virus from HHV-1 (HSV-1) to HHV-8 is involved. Many of these are practically endemic in humans, but commonly remain latent for most of a lifetime. This points to an acquired defect in the mechanisms which hold viral infections latent. Most people who are seriously ill with this disease have multiple active (but not acute) viral infections. Many of these are HHVs, like EBV, CMV, VZV, but not all. Parvoviruses, adenoassociated viruses and bocaviruses are examples of other DNA viruses you may see. Enteroviruses are examples of RNA viruses which sometimes cause these symptoms. If all these are not separate and unrelated diseases there appears to be a fundamental acquired immune defect which (usually) remains limited, unlike AIDS. Limited immunosuppression is the clue which makes me consider retroviruses seriously.

I feel the need at this point for a disclaimer, I do not believe the course of the infection is the same in all people. I am now convinced that over 90% of those infected generally remain asymptomatic, except in cases where some other insult damages immune response. In those exceptions, there is always some confounding factor which can be blamed. Our political problem is that 90+% of the population is not especially vulnerable, most of the time. What happens when they grow old is another matter entirely. The similarity between our symptoms and those of aging people convinces me many more people are affected at some stage in life. Connect the dots, and political will should follow.

What is your take on limited immunosupression stemming from prenatal maternal infection? Infection in some stages of pregnancy can skew fetal immune system for good, ie have life-long effects. At least in animals. This is suspected to play a role in schizo, and looks very likely to play a major role in autism. This model would not necessarily push retroviruses out of the picture. Not sure how it would fit late onset ME though. Thoughts?

from
http://forums.phoenixrising.me/inde...eads-to-permanent-immune-dysregulation.18523/

... Next, the researchers characterized the immune system of the offspring of mothers that had been infected and found that the offspring display a number of immune changes. Some of those changes parallel those seen in people with autism, including decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Taken together, the observed immune alterations add up to an immune system in overdrive—one that promotes inflammation.

“Remarkably, we saw these immune abnormalities in both young and adult offspring of immune-activated mothers,” Hsiao says. “This tells us that a prenatal challenge can result in long-term consequences for health and development.”

 

[anciendaze]

The problem of maternal environment influence is complicated. Part of this is that too strong an influence will produce such drastic changes the fetus will be destroyed. This may actually happen in miscarriages and stillbirths. The well-adapted infections I am now considering would need to avoid this, because transmission around the time of birth (perinatal) is a major route of transmission in many species. It is important that any pathogen transmitted at sexual maturity not put itself out of business earlier. When HIV actively infects children it is revealing its inexperience in a new host species. Without a great deal of medical technology those children would never survive to sexual maturity.

Transmission via the placenta is a problem because the child's immune system is very imperfect. Distinguishing "self" from "other" doesn't make much sense when "other" is mother. A number of known problems develop precisely because of a mismatch between child and maternal immunity.

The best opportunity for any pathogen would be postnatal infection while the infant immune system is still naive, provided this does not kill the neonate. In several species the pathogen is transmitted via milk. There is confusion on this subject because milk is typically loaded with maternal antibodies which disable free virions. What I believe is going on is the transmission of a latent infection via infected maternal immune cells which make direct contact with dendritic cells (DC) in the mucosa of the infant gut. These then move to lymphatic organs. Dendritic cells can hold a virus in a separate compartment without being infected themselves. Once the virus has been passed this way it can then be passed directly to T-cells, or other immune cells, without being exposed in the bloodstream. Active virus can be destroyed by antibodies produced by the mother. This selects for cells with latent infections.

This complicated, and downright weird, sequence of events is the only one I've come up with which allows a latent infection to be passed from mother to child without producing an active infection in offspring until hormone changes signal sexual maturity. There is laboratory evidence, e.g. on MMTV, making this more than pure speculation, but not every link in the chain is solid.