Anergy and chemokine receptors.

The human immunodeficiency virus (HIV) induces a spectrum of immune abnormalities in the host by binding to CD4 molecules and chemokine receptors. Anergy, apoptosis, and immune activation are among the diverse immunological changes observed in the host. Chemokines, being the natural ligands for the chemokine receptors, block the entry of a retroviral strain, which exhibits tropism for the given receptor. This opens new therapeutic strategies and intervention possibilities for treating HIV infected individuals.

Anergy and chemokine receptors.

The human immunodeficiency virus (HIV) induces a spectrum of immune abnormalities in the host by binding to CD4 molecules and chemokine receptors. Anergy, apoptosis, and immune activation are among the diverse immunological changes observed in the host. Chemokines, being the natural ligands for the chemokine receptors, block the entry of a retroviral strain, which exhibits tropism for the given receptor. This opens new therapeutic strategies and intervention possibilities for treating HIV-infected individuals.

Anergy and acquired immune deficiency syndrome.

Human immunodeficiency virus (HIV), the retrovirus associated with acquired immune deficiency syndrome (AIDS), acts as a super-antigen by binding to the variable region of the beta (V beta) chain of T-cell receptor (TCR). It's binding to CD4 molecules and chemokine receptors induces a spectrum of immune abnormalities including 'a state of anergy' in the host. This state is due to a defective function of T-helper cell-1 (Th-1), a reduction in production of lymphokines required for signal transduction, an impaired cytotoxic cell activation and a decrease in antigen presenting function of monocyte-macrophage cell lineage. These immune abnormalities form the basis for severe opportunistic infections and malignancies in the host. Malnutrition, micronutrient abnormalities, concomitant infections and genetic factors, etc., are some of the compounding co-factors that further contribute to 'the state of anergy'.

Anergy and human immunodeficiency virus infection.

Human immunodeficiency virus (HIV), the retrovirus associated with acquired immune deficiency syndrome (AIDS), induces a spectrum of immune abnormalities including a state of anergy in the host. This state is due to the binding of HIV envelope glycoprotein moieties to CD4 molecules and chemokine receptors. Resulting decrease in antigen presenting cell function and the interference with functioning of positive and negative regulatory molecules involved in signal transduction have an anergizing effect on the immune system. This effect is exemplified by diminished production of interleukin-2 (IL-2) and interferon-gamma and reduced expression of IL-2 receptor by CD4 helper cells of HIV patients. These immune abnormalities lead to clinically relevant immunological phenomena such as Type-1 to Type-2 switch, decrease in delayed-type hypersensitivity dermal reaction, etc. Insight into these interesting phenomena could pave the path for favorably altering the immunological milieu for drug and vaccine trials.

Nutrients as modulators of anergy in acquired immune deficiency syndrome.

Malnutrition induces a spectrum of immune abnormalities including a state of anergy in the host. This state is due to a decrease in CD4 + helper cells, diminished cytotoxic cell activity and reduction in production of lymphokines required for signal transduction. Human immunodeficiency virus (HIV), the retrovirus known to cause acquired immune deficiency syndrome (AIDS), leads to a state of anergy by causing similar immunological changes. Micronutrient abnormalities, concomitant infections and genetic factors, etc., are some of the compounding co-factors which further contribute to the deterioration of the immune functions in AIDS patients. Reversal of these immune abnormalities would improve the quality of life of HIV-infected individuals.

Anergy, AIDS and tuberculosis.

Human immunodeficiency virus causes an immunological 'state of anergy'. This state is due to a defective function of antigen-presenting cells, a depletion of CD4+ helper cells, a reduction in the production of soluble factors required for signal transduction, and a decrease in cytotoxic cell activation. The human immunodeficiency virus epidemic has resulted in a global resurgence of tuberculosis. Tuberculin skin testing is negative in 58% of the patients with acquired immunodeficiency syndrome who develop tuberculosis. The mechanism leading to a state of anergy and the mechanism leading to dissemination of dormant tuberculosis appear to be identical.

Acro-pectoro-renal field defect with contralateral ureteropelvic junction obstruction.

Ureteropelvic junction obstruction was noted in a newborn male infant with acro-pectoro-renal field defect. To our knowledge, this association has not previously been reported. Ultrasonography of the urinary tract should be performed on all children with aplasia of the pectoralis major muscle.

Mechanism of anergy in AIDS and malnutrition.

Human immunodeficiency virus, the retrovirus associated with acquired immunodeficiency syndrome, is known to deplete CD4+ helper cells and reduce CD8+ cytotoxic cell activity, resulting in impaired cell-mediated immunity and a 'state of anergy'. This leads to dissemination of micro-organisms that are normally held dormant in the host by the cell-mediated immune system. Malnutrition also leads to depletion of CD4+ helper cells and decreases CD8+ cytotoxic cells leading to impaired cell-mediated immunity and 'state of anergy'. Clinical situation can worsen when the two conditions co-exist.

Aplasia of pectoralis major muscle and renal anomalies.

We describe two patients with aplasia of the pectoralis major muscle and renal anomalies. We think such an association, which has been reported previously, represents a new congenital malformation, probably not a syndrome but an acro-pectoro-renal field defect. We recommend renal ultrasonography be done on all children with aplasia of the pectoralis major.

Skull erosion and bony changes in a child with endocardial cushion defect.

A 9-year-old boy with an endocardial cushion defect who had skull erosion as well as widening of the diploe is described. This was accompanied by thickening of the tables, "hair-on-end" striations in the skull, and cortical thinning and medullary cavity expansion in the femora. The skull erosion is attributed to venous distension and increased blood volume. The finding of skull erosion in cyanotic congenital heart disease has not been reported before.