HIV begins its Life cycle by gluing to a cell of it's host usually the CD4 receptor on the host cell (
also known as T4 lymphocyte). Following fusion of the virus with the host cell, HIV
enters the cell. The genetic material of the virus, which is RNA, is released
and undergoes reverse transcription into DNA. An enzyme in HIV called reverse
transcriptase is necessary to catalyze this conversion of viral RNA into DNA. At
this moment antiretroviral drugs under the
Nucleoside analogues
HIV CELL
and non Nucleoside analogues such as the the
Azidothymidine (AZT), will inhibit the growth of the virus at this level.
Once the genetic material of HIV has been changed into DNA, this viral DNA
enters the host cell nucleus where it can be integrated into the genetic
material of the cell. The enzyme integrase catalyzes this process, and
inhibitors of integrase are under study as a new way to block HIV replication.
Once the viral DNA is integrated into the genetic material of the host, it is
possible that HIV may persist in a latent state for many years. This ability of
HIV to persist in certain latently infected cells is the major barrier to
eradication or cure of HIV. Activation of the host cells results
in the transcription of viral DNA into messenger RNA (mRNA), which is then
translated into viral proteins. The new viral RNA forms the genetic material of
the next generation of viruses. The viral RNA and viral proteins assemble at the
cell membrane into a new virus. Amongst the viral proteins is HIV protease,
which is required to process other HIV proteins into their functional forms.
Protease inhibitors, one of the most potent types of anti-viral medications, act
by blocking this critical maturation step. Following assembly at the cell
surface, the virus then buds forth from the cell and is released to infect
another cell.