BIOC31H3 Lecture Notes - Azide, Reverse Transcriptase, Mutation Rate

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Sustained immune activation during hiv infection can ultimately deplete the body"s supply of helper t cells and lead to the collapse of the host"s defences. An untreated hiv infection exhibits distinct phases, in which the loss of helper t cells happens at different rates and appears to be driven by different mechanisms. In the acute or initial, phase, hiv virions enter the host"s body and begin to replicate. Hiv gains entry into a host cell by first latching onto the cell-surface protein cd4, then binding to a coreceptor. The coreceptor used by most of the hiv strains responsible for new infections is ccr5: these viral strains can thus infect dendritic cells, macrophages, regulatory t cells, and especially memory and effector helper t cells. The acute phase ends when viral replication slows and the concentration of virions in the blood drops: this slow down may be because that the virus simply runs short of host cells it can easily invade.

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