Which one of the following is true regarding HIV infection -
Pathogenesis of HIV infection and AIDS
Primary infection of cells through the blood and mucosa. 

The initial entry of the virus may be through a mucosal surface, as in sexual intercourse (via rectal or cervical mucosa) or via blood exposure e.g. (after intravenous drug abuse).
From the mucosa the virus is carried to the regional lymph nodes by dendritic cells while the virus initially inoculated into the blood is rapidly cleared by the spleen and lymph nodes.
Thus, with either mode of entry, the virus initially replicates in the lymphoid organs and then spills over into the blood.

Infection established in lymphoid tissue e.g, lymph node

After the infection is established in the lymph node the virus spills into the blood the patient will now experience the acute HIV syndrome.

Acute HIV syndrome, the spread of infection throughout the body

This phase is characterized initially by high levels of virus in plasma and widespread seeding of the virus in lymphoid tissues.
Sometimes there is an abrupt reduction in CD4+ T cells.
During this period, the HIV virus can be readily isolated from the blood, and there are high levels of HIV p24 antigen in serum.
Soon, however virus specific immune response develops

Immune response

The viremia is readily controlled by the development of an antiviral immune response.
It is estimated that 40% to 90% of individuals who acquire a primary infection develop the viral syndrome 3-6 weeks after infection and this resolves spontaneously in 2 to 4 weeks.
The resolution of viremia occurs due to the immune response.
Virus-specific antibodies develop evidenced by seroconversion (usually within 3-7 weeks of presumed exposure) and more importantly virus-specific CD8+ cytotoxic T cells also develop.
HIV specific CD8+ T cells are detected in the blood, at this time, viral titres begin to fall and are most likely responsible for containment of HIV infection.
As viral replication stops CD4+ T cells return to near normal numbers, signalling the end of the acute phase.

Clinical Latency

The clinical latency or the middle chronic phase represents a stage of relative containment of the virus.
Although the plasma viremia declines, there is widespread dissemination and seeding of the virus, especially in the lymphoid organs.
The viral load at the end of the acute phase reflects the equilibrium reached between the virus and the host after the inital battle and in a given patient may remain fairly stable for several years.
This level of steady state viremia, or the viral "set point" is a predictor of the rate of decline of CD4+ T cells and therefore progression of HIV disease.
In one study, only 8% of patient with a viral load of less than 4350 copies of viral mRNA/ 1 progressed to full blown AIDS in 5 years, where as 62% of those with a viral load of greater than 36, 270 copies had developed AIDS in the same period.
From a practical standpoint, therefore the extent of viremia, measured as IIIV-tRNA is a useful surrogate marker of HIV disease progression and is of clinical value in the management of people with HIV infection.
However, in patients treated with highly active antiretroviral therapy (HAART), clinical improvement is often greater than the decrease in plasma viremia and it is generally accepted that virenzia as well as the blood CD4+ T cell counts should be considered in the management.
Regardless of the viral burden, during the middle or chronic phase, there is continuing battle between HIV and the host immune system.
The CD8+ cytotoxic T cell response remains activated and extensive viral and CD4+  cell turnover continues.
However, because of immune regenerative capacity of the immune system a large proportion of the lost CD4+ cells is replenished.
Thus the decline in CD4+ cell count in blood is modest.
After an extended variable period, there begins a gradual erosion of CD4+ T cell and full blown AIDS ensues AIDS
In this phase the host defence begins to wane.
There is loss of CD4+ T cells.
Concomitant with this loss, the proportion of the HIV virus in the blood increases.
It is characterized by a breakdown of the host defence, a dramatic increase in plasma virus and clinical disease.
Typically the patient presents with long lasting fever (> 1 months), fatigue, weight loss and diarrhoea.
After a variable period, serious opportunistic infections, secondary neoplasms or clinical neurological disease (grouped under the rubric AIDS indicator disease, discussed below), supervene and the patient is said to have developed AIDS.
It should be evident from our discussion that in each of the three phases of HIV infection, viral replication continues to occur .
Even in the chronic phase, before the severe decline in CD4+ cell count and the development of AIDS, there is extensive turnover of the virus.
In other words HIV infection lacks a phase of true microbiologic latency, thus it is a phase during which all the HIV is in the form of proviral DNA and no cell is productively infected.
Following needle stick injury infectivity is reduced by adminsitration of nucleoside analogues
CD4 counts are the best predictors of disease progression
Infected T cells survive for a month in infected patients
In latent phase HIV has minimal replication