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Paul Simmons

So if I correctly understand your summary, the presenters were NOT saying that these HERVs play a role in pathogenesis; but rather that they might serve as a surrogate for identifying and eliminating HIV-infected cells. Yes?

Richard Jefferys

Hi Paul, as far as I understand it that's correct, the endogenous viruses can't become replication-competent and do any damage themselves, but - according to these researchers - they do seem to be able to make proteins inside HIV-infected cells and thus targeting these endogenous proteins could offer the immune system an alternative way of targeting HIV-infected cells. I think a lot more work will have to be done to show if this is really possible.

Brad Jones

Thanks for your interest, and a very accurate summary of our work!

To address Paul and Richard's comments - we do feel that it is likely that aberrant activity of these elements in the context of natural HIV-1 infection does contribute to pathogenesis. However, further insight into their behaviour in that context is necessary before proposing any mechanisms i.e: one very important question is whether or not retrotransposition is strictly limited to HIV-1 infected cells. If so, this naturally sets limitations on any potential contribution to pathogenesis (but adds weight to the argument that these antigens can be used as surrogate markers of HIV-1 infected cells).

The inverse question which I find interesting, if a bit more abstract, is whether the retrotransposition of these elements could play a defensive role in retroviral infection i.e: the HIV-1 sequence containing the LINE-1 insertion that I pointed out in my talk, has essentially been inactivated by the LINE-1 element (as Vif, Vpr, Tat, and Rev are all deleted). Could newly inserted retroviruses potentially serve as hotspots for integration of endogenous elements - leading to distruption of the invasive virus?

Richard Jefferys

Thanks for the information & clarification Brad, very interesting work!

Pat Kramme

Great comments! Endogenous retroviruses have been characterized in many species, feline, chicken, mouse, long before HIV. While they are generally not replication competent it is possible for them to act as loci of recombination with other retorviruses. In addition, replication incompetent viruses often become replication comeptent when there is co-infection with a replication competent retroviruses, e.g., tumor causing retorviruses such as Rous sarcoma virus. Usually this occurs between closely related retroviruses with the same or similar RNA sequences that facilitate incorporation into a virion. Are human endogenous retroviruses related to lentiviruses (HIV) or are they more typical of tumor viruses (alpha, beta, gamma, or spumiviruses)?

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