Clinical Course of HIV Infection

The course of HIV disease can be followed by measuring the amount of virus in the patient's plasma and by the blood CD4+ T cell count (see Fig. 20-8).

• The acute phase of the illness, also called the acute HIV syndrome, is the period of viremia characterized by nonspecific symptoms of infection. It develops in 50% to 70% of infected adults typically 3 to 6 weeks after infection. There is a spike of plasma virus and a modest reduction in CD4+ T cell counts, but the number of blood CD4+ T cells often returns to normal. In many patients, however, the infection is occult and there are no symptoms.

• The chronic phase of clinical latency may last for many years. During this time, the virus is contained within lymphoid tissues, and the loss of CD4+ T cells is corrected by replenishment from progenitors. Patients are asymptomatic or suffer from minor infections. Within 2 to 6 months after infection, the concentration of plasma virus stabilizes at a particular set-point, which differs among patients. The level of the viral set-point and the number of blood CD4+ T cells are clinically useful predictors of the progression of disease. As the disease progresses, patients become susceptible to other infections, and immune responses to these infections may stimulate HIV production and accelerate the destruction of lymphoid tissues. As discussed earlier, HIV gene transcription can be enhanced by stimuli that activate T cells, such as antigens and a variety of cytokines. Cytokines, such as TNF, which are produced by the innate immune system in response to microbial infections, are particularly effective in boosting HIV production. Thus, as the immune system attempts to eradicate other microbes, it brings about its own destruction by HIV.

• HIV disease progresses to the final and once almost invariably lethal phase, called AIDS, when the blood CD4+ T cell count drops below 200 cells/mm3. HIV viremia may climb dramatically as viral replication in reservoirs other than T cells accelerates unchecked. Patients with AIDS suffer from combinations of opportunistic infections, neoplasms, cachexia (HIV wasting syndrome), kidney failure (HIV nephropathy), and CNS degeneration (AIDS encephalopathy) (Table 20-7). Because CD4+ helper T cells are essential for both cell-mediated and humoral immune responses to various microbes, the loss of these lymphocytes is the main reason that patients with AIDS become susceptible to many different types of infections. Furthermore, many of the tumors that arise in patients with AIDS have a viral etiology, and their prevalence in the setting of AIDS reflects an inability of the HIV-infected patient to mount an effective immune response against oncogenic viruses. Cachexia is often seen in patients with chronic inflammatory diseases and may result from effects of inflammatory cytokines (such as TNF) on appetite and metabolism. The CNS disease in AIDS may be due to neuronal damage by the virus or by shed viral proteins such as gp120 and Tat, as well as the effects of cytokines elaborated by infected microg-lial cells. Many of these devastating consequences of HIV infection, including opportunistic infections and tumors, have been significantly reduced by highly active antiretroviral therapy.

TABLE 20-7 Clinical Features of HIV Infection

Phase of Disease

Clinical Feature

Acute HIV disease

Fever, headaches, sore throat with pharyngitis, generalized lymphadenopathy, rashes

Clinical latency period

Declining blood CD4+ T cell count

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