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People infected with human immunodeficiency virus type 1 (HIV-1) but show no apparent progression of the disease appear to have a relatively low viral load and their lymph nodes and immune functions appear to remain effective. A percentage of people infected with HIV-1 show no progression of the disease for years. A study compared 15 of these patients, who had been infected at least 7 years, with 18 patients with progressive HIV disease. The lymph nodes of the non-progressive patients did not show the large germinal centers, follicle lysis, hyperplasia and lymphocyte depletion found in the nodes of the progressive patients. HIV-1 levels in plasma and peripheral-blood mononuclear cell were significantly lower for the non-progressive patients, who also had higher tithers of neutralizing antibodies than were found in the progressive subjects. Replication of the virus was found in the lymph nodes of the non-progressive patients, however.

Combined semiquantitative polymerase chain reaction assay and cytofluorometry analysis of T-cell antigen receptor in sequential peripheral blood mononuclear cells of HIV patients who express the T-cell regulated primary immune response to HIV revealed major oligoclonal elongation of variable domain beta-chain (V-beta) families. These cells with expanded V-beta represented the CD8 T-cell differentiation antigen and regulated HIV-specific cytotoxicity. These expansions indicate a vital constituent of the primary immune response to viral infections and explain the immunopathogenic and protective mechanisms of HIV infection.

A study of the T-cell receptor beta-chain variable-region (V(sub beta)) repertoire in monozygotic twins discordant for human immunodeficiency virus demonstrated disruptions of specific V(sub beta) segments in CD4+ T cells of the virus-positive twins. Members of the V(sub beta)21 family were disrupted in four out of seven instances, and those of the V(sub beta)13 family were disrupted in six out of the seven instances examined.

Researchers investigated the frequency of human immunodeficiency virus type 1 (HIV-1) infected cells, or the kinetics of viral burden, and replication during primary and early-chronic infection in the peripheral blood mononuclear cells (PBMC) of four severely affected persons. The down-regulation in the extent of virus replication related to the clinical transition from acute to chronic infection does not unconditionally imply a decrease in viral burden since other elements may be involved.

The location of the human immunodeficiency virus (HIV) during the course of infection was monitored in AIDS patients at various stages of the disease using polymerase chain reaction techniques. The results showed that HIV is preferentially localized at the lymphoid tissue during the early course of infection. At the intermediate stage, the virus is trapped in selected germinal centers of the follicular dendritic cells of lymph nodes. At the late stages of the disease, the virus is released from the lymph tissue to the peripheral blood mononuclear cells.

Infection with the human immunodeficiency virus (HIV) follows a characteristic course of prolonged latency followed by the onset of minor signs and symptoms, AIDS-defining disease and death. Following infection, 50% to 70% of patients develop a mononucleosis-like syndrome and then generally have few clinical symptoms during latency, which lasts an average of 10 years. During this time, the virus undergoes considerable replication in the lymphoid organs, and circulating CD4 T cells, which are a type of white blood cell, are gradually depleted. The eventual onset of AIDS following the deterioration of the immune system is usually marked by the appearance of an opportunistic infection or cancer. HIV is thought to directly mediate cell death, but other proposed mechanisms of CD4 T cell depletion include HIV-specific immune responses, autoimmune mechanisms and programmed cell death. In the late stages of disease, the lymphoid organs, which appear to function as HIV reservoirs, may no longer be able to contain the virus particles, and may release them into circulation.

The effect of retinoic acid (RA) on human immunodeficiency virus (HIV) expression in acute and chronically infected mononuclear phagocytes was investigated and analyzed. RA was found to inhibit HIV transcription and virus expression in promonocytic U1 cells in a manner similar to that exhibited by transforming growth factor beta (TGF-beta). Despite its close parallel to TGF-beta-induced effects, RA-induced inhibition was found to be independent of TGF-beta mediation. These results prove that while long-term TGF-beta administration is not feasible due to its short half- life, RA, which exerts similar effects, may be used as substitute in the management of HIV infection.

Changes in the microbiota are associated with disease susceptibility, immune system development, and responses to treatment. Refocusing research to elucidate the causal links between the human microbiota and infectious and immune-mediated diseases will be critical to harnessing its power to prevent, diagnose, and treat such diseases. [ABSTRACT FROM AUTHOR]

The human T-lymphotropic virus type I (HTLV-I) is associated with adult T-cell leukemia and a neurological (affecting the nervous system) disease of the spinal cord called tropical spastic paraparesis or HTLV-I-associated myelopathy. Tropical spastic paraparesis or HTLV-I-associated myelopathy is a chronic condition where the myelin which surrounds the nerves (primarily the nerves of the spinal cord) degenerates, resulting in muscle weakness and loss of sensory function. However, only 1 percent of individuals who are infected with HTLV-I develop any clinical signs of disease. This difference in the development of disease among individuals may be associated with the following: the genetic backgrounds of the individuals; differences in the strains of virus causing the infection; and the immune response of the individuals to the virus. The individual differences in the immune response to HTLV-I were examined. It was found that individuals with neurological disease had high levels of a type of T lymphocytes, known as CD8+ cells, that are cytotoxic to (can kill) cells containing HTLV-I. These high levels of CD8+ cells were not seen in individuals who had antibodies to HTLV-I, indicative of infection, but did not have neurological disease. It is thought that HTLV-I specific cytotoxic T lymphocytes may contribute to the disease state in the neurological disorder tropical spastic paraparesis or HTLV-I-associated myelopathy. (Consumer Summary produced by Reliance Medical Information, Inc.)

Author(s): Anthony S Fauci [1] Over the past decade, issues related to the health of people in resource-poor countries have captured the attention of world leaders, governments, philanthropies, policy makers [...]