HIV1 specific humoral immune responses

The association between an HIV-1-specific humoral immune response and the course of disease is less well characterized.

In a SIV model, injection of an antibody cocktail consisting of various neutralizing antibodies is able to prevent SIV infection after a mucosal virus challenge (80), indicating that primary protection is mainly dependent on a broad humoral immune response. In contrast, B cell depletion by a monoclonal antibody directed against B cells in monkeys with already established SIV infection, does not affect the course of plasma viremia (81).

A slow progression of immunodeficiency was observed in patients with high titers of anti-p24 antibodies (82), persistence of neutralizing antibodies against primary and autologous viruses (83), and lack of antibodies against certain gp120 epitopes (84).

Long-term non-progressors with HIV tend to have a broad neutralizing activity towards a range of primary isolates and show persistence of neutralizing antibodies against autologous virus. At present, it is unclear whether the presence of neutralizing antibodies in LTNP represents part of the protection or whether it merely reflects the integrity of a relatively intact immune system. Individuals that have a substantial risk for HIV-1 infection, but are considered "exposed, non-infected", by definition represent individuals with a lack of a detectable antibody response to HIV-1. This definition implies that a systemic humoral immune response may not represent a crucial protective mechanism. It has been shown that these individuals may demonstrate a local (mucosal) IgA response against HIV-1 proteins that are not detected by the usual antibody testing methods (85). Thus, local IgA, rather than systemic IgG, may be associated with protection against HIV-1 infection. There is also some evidence that some anti-HIV-1 antibodies can enhance the infection of CD4 T cells.

A number of old and recent studies have shown that neutralizing antibodies do exist in HIV-1-infected individuals, however, there is a time lag in their appearance. That is, individuals will develop neutralizing antibodies to their own viruses with time, however, by the time these antibodies develop, the new viruses circulating in the individual's plasma will become resistant to neutralization, even though the older ones are now sensitive to the current antibodies in the patient's serum. Thus, the antibody response appears to be hitting a 'moving' target, allowing viruses to escape continuously. Further knowledge gained on understanding the mechanisms of humoral escape will likely lead to potential new therapies.

Improved knowledge and understanding of the pathophysiological mechanisms during the course of HIV-1 infection have not only contributed to the development of antiretroviral treatment strategies, but have given rise to new therapeutic approaches, such as cytokine therapies, e.g., IL-2 and therapeutic vaccination. However, the most important challenge and thus, the demand for a better understanding of the immunopathogenesis of HIV-1 infection, remains the development of a protective vaccine, which is urgently needed to interrupt the epidemic especially in countries of the Sub-Sahara and Southeast Asia.

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