Regarding how the presence of herpes might effect, one's risk of getting HIV from a needle stick, those are likely to be independent risk factors and while they may interact, the amount of interaction in the situation you mention is likely to be less inportant that the characterisitics of the needle stick and the person from whom the needle stick was received.
The interactions involve both the location of the herpes infection as well as the type of virus (HSV-1 or-2). As I said before, the effect of HSV-1 infections is not well studied and studies are complicated by the fact that a person with HSV-1 could be infected at either site.
To be honest, as I've already mentioned, there is a lack of data on HSV-1/HIV interactions and the interactions are complex to a level beyond the intended focus of this site. I hesitated to even try to explain about it as I started to answer your question. To answer it fully and completely would take pages written at a releatively high scientific level and even then there would still be a substantial amount of inference involved. I think it best to not try to go beyond what I've already said. EWH
if I have HSV-1 on my lips would that increase my chances of contracting HIV as much as having HSV-1 on my genitals when no symptoms were apparent in either place?
So having herpes would increase the risk of getting HIV for a person who got a needle stick with infected blood even if it stuck them in the finger?
Dr. Handsfield and I share the forum. You got me. FYI, the reason we share the forum is because we have worked together for nearly 30 years and while our verbiage styles vary, we have never disagreed on management strategies or advice to clients.
There is less information about the change in risk for HIV occurring in persons with HSV-1 than there is for persons with HSV-2. That said, the viruses are closely related and act similarly biologically so it is reasonable to think that they affect HIV risk similarly, that is to increase it. The reasons that HIV risk is increased in persons with HSV-2 is thought to be for two reasons - due to the presence of recurrent lesions acting as a "doorway" to make the virus more easily introduced into the body as well as through a less well understood immunological reaction in which the herpes "primes" the immune system to be ready to get infected by HIV. Both of these are likely to be active, to some degree in persons with HSV-1 as well. The relationship has been harder to study however because so much of HSV-1 is oral rather than genital infection so determining the site of infection in large enough groups to generate meaningful data is difficult.
The available data does not suggest that the severity of one's herpes changes the risk.
The increase in risk is not as great as the risk as much as an HIV contaminated needle stick would. EWH