The virus has cytopathic effects but how it does it is still not quite clear. It can remain inactive in these cells for long periods, though. This effect is hypothesized to be due to the CD4-gp120 interaction.

• The most prominent effect of HIV is its T-helper cell suppression and lysis. The cell is simply killed off or deranged to the point of being function-leapses leading to the familiar AIDS complications, like infections and neoplasms (vide supra).

• Infection of the cells of the CNS cause acute aseptic meningitis, subacute encephalitis, vacuolar myelopathy andperipheral neuropathy. Later it leads to even AIDS dementia complex.

• The CD4-gp120 interaction is also permissive to other viruses like Cytomegalovirus, Hepatitis virus, Herpes simplex virus, etc. These viruses lead to further cell damage i. e. cytopathy.

It is important to distinguish between identifying among whom new infections are predicted to occur in the short term, which the model does, and the types of risk behaviour that sustain the epidemic (i.e. the epidemic drivers).31 For example, although a large proportion of new HIV infections may occur among individuals in serodiscordant, stable, monogamous partnerships, the index HIV-positive partners in these couples may have previously acquired the infection through higher-risk behaviour, such as commercial sex. Currently, both partners would be classified as part of the low-risk population, but the essential driver of HIV transmission between the partners is previous sexual contact within commercial sex networks. This is an important distinction, particularly when the model results are used for planning prevention programmes, which may then under allocate resources for prevention in commercial sex settings. Allocating resources for prevention to match the predicted distribution of new infections identified in the MOT analysis implicitly focuses prevention efforts on reducing the risk of acquisition among susceptible individuals. However, in some cases, it may be more effective