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From early in the human immunodeficiency virus (HIV) pandemic it was noted that a long subclinical latent phase preceded the appearance of opportunist infections. The use of immune monitoring to prompt prophylactic agents considerably reduced morbidity caused by opportunist infection1 in the 1980s. In the past few years, as new antiretroviral treatments emerged but were threatened by resistance, viral monitoring has been used to guide such treatment. Consensus guidelines on laboratory monitoring2,3 and treatment4 in HIV have been published on both sides of the Atlantic. In this article, we discuss the natural history of HIV infections, current immunological and virological tests, and recommendations for monitoring protocols.J Clin Pathol 2000;53:266–272
Natural history of HIV infection
Efficient infection of T helper cells, macrophages, and dendritic cells by HIV requires expression of the CD4 molecule and chemokine receptors. In early infection, HIV is characteristically trophic for the CCR5 chemokine receptor on macrophages and dendritic cells, explaining why the 1% or so of the white population with a CCR5 polymorphism are relatively protected from HIV.5
Early HIV infection is characterised by active viral replication, with high amounts of viral RNA, recoverable virus, or viral antigens such as p24 being found.6 Subsequently, viraemia falls because specific cytotoxic T cells kill infected cells, replication is inhibited by non-lytic means, or the availability of uninfected target cells is exhausted.7,8 Thus, an initial precipitous fall in CD4+ cell counts may be followed by partial recovery at this stage.
Although the amounts of virus in blood fall, replication continues in lymphoid tissue9 until a new steady state of viraemia is attained. The mean half life of the virus in the plasma is approximately two days,10,11 suggesting that the continual production of virus and target cells is matched by an equivalent rate of …