Kralen infecting cells. Where does the membrane of the HIV virus, which may contain a lipid membrane, likely derive? It is acquired upon release from the previously infected cell membrane. It is acquired through the translation of the newly infected cell. It is acquired from the cytoplasm. It is acquired upon endocytosis and entry into the next cell. HIV infection, regardless of exposure, affects these individuals. Some patients are known to be resistant to the virus, but it is not clear if they truly have physiological resistance or if they are simply lucky. They hypothesize that these patients have hyper-reactive cytotoxic cells that recognize infected helper cells quicker than the average person. Presumably, these cells would lead to a quicker response and reduction in the amount of viral load present in these individuals. If this hypothesis is true, then the following statements are likely not true: hyper-reactive cytotoxic cells would not have viral particles in their system even after exposure, hyper-reactive cytotoxic cells would likely block the reverse transcriptase process in infected helper cells, and hyper-reactive cytotoxic cells would induce apoptosis in the infected cells quicker than normal. The following statements are likely true: the MHC activity of the cells will present viral particles on the cell surface, the cells will continue to produce viral particles until they are killed, and the cells will have more genome than normal cells. Doctors have also determined that aspirin may be able to assist in preventing the contraction of HIV through vaginal sex. HIV transmission has been linked to penile swelling and lesions within the squamous epithelium of the vagina and penis. In women that take aspirin regularly, however, this swelling is reduced. In doing so, the HIV virus is less likely to make it into the system. Aspirin, in this example, prevents inflammation within the genitals.