HIV induced AIDS and related cancers: chronic immune activation and future therapeutic strategies.

Chronic generalized immune activation represents one of the most critical features determining progression to AIDS. This may result in the manifestation of malignancy, with lymphoma and Karposi's sarcoma being the first to be recognised. In this regard, the manifestation of lymphoma is very similar to that seen in transplant patients and those with graft versus host disease (GVHD) where both chronic immune activation and immune suppression are present.

HIV immunopathogenesis and strategies for intervention.

Therapeutic options aimed at tackling the HIV pandemic face many obstacles. The lack of readily accessible and affordable therapies means that most of those affected go untreated. The array of escape mechanisms used by HIV has undermined the efficiency of many antiviral products and continually represents a barrier to the development of an effective vaccine.

Pathogenesis of HIV: non-specific immune hyperactivity and its implications for vaccines.

More than a decade ago, the pathogenesis of AIDS was reviewed in this journal, using the subtitle 'classical and alternative views', when evidence was accumulating that HIV could not cause AIDS simply through direct cytopathic mechanisms alone. Generalised immune activation after infection with HIV is now understood to be associated with and predictive of disease progression and probably represents the single most important difference between rapid progression and slow or non-progression. However, the fundamental source of this phenomenon remains undetermined.

HLA homology within the C5 domain promotes peptide binding by HIV type 1 gp120.

The mechanisms by which HIV-1 induces chronic pathogenic immune activation associated with disease progression remain unclear despite many years of AIDS research. One proposal suggests that sequence and structural mimicry between gp120 and HLA may endow HIV with the capacity to arouse alloreactive and autoimmune responses within the susceptible host, fueling disease progression in a manner similar to graft-versus-host disease (GVHD). Both gp120 and HLA share a common functional interaction with CD4 but also demonstrate peptide binding properties.