Related Experiment Video
Updated: Aug 14, 2026

Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
The immunocompromised host: HIV infection
1Division of Pulmonary and Critical Care Medicine (111G), University of Michigan Medical School, and Medical Service, Department of Veterans Affairs Medical Center, 2215 Fuller Road, Ann Arbor, MI 48105, USA. jamebeck@umich.edu
Abstract:
The variety of pulmonary infections encountered in HIV-infected individuals indicates that many components of the host defense network are impaired. In addition to depletion of CD4+ T cell numbers, HIV infection results in functional deficits in CD4+ T cells, CD8+ T cells, and natural killer cells. Although some components of macrophage defense are preserved, lack of activation signals from CD4+ T cells contributes to impaired defense by macrophages. There are few data examining the functional capabilities of neutrophils in the lung, but evidence from peripheral blood neutrophils indicates that defense by these cells is also impaired. An improved understanding of these events in the lung during HIV infection could lead to specific interventions aimed at restoration of deficient function.
Related Concept Videos
Immunodeficiency Diseases
There are three main causes of immunodeficiency disorders...
Sexually Transmitted Infections
Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
Cryptococcal Meningitis
Factors Affecting the Risk of Infection
The integrity and count of the white blood cells help the body resist pathogens and fight infection. When impaired, it reduces the body's resistance to pathogens. The acidic pH levels of the gastrointestinal, genitourinary tracts, and skin create...
Cytomegalovirus Disease
