SIV Infection of Lung Macrophages.
HIV-1 depletes CD4+ T cells in the blood, lymphatic tissues, gut and lungs. Here we investigated the relationship between depletion and infection of CD4+ T cells in the lung parenchyma. The lungs of 38 Indian rhesus macaques in early to later stages of SIVmac251 infection were examined, and the numbers of CD4+ T cells and macrophages plus the frequency of SIV RNA+ cells were quantified. We showed that SIV infected macrophages in the lung parenchyma, but only in small numbers except in the setting of interstitial inflammation where large numbers of SIV RNA+ macrophages were detected. However, even in this setting, the number of macrophages was not decreased. By contrast, there were few infected CD4+ T cells in lung parenchyma, but CD4+ T cells were nonetheless depleted by unknown mechanisms. The CD4+ T cells in lung parenchyma were depleted even though they were not productively infected, whereas SIV can infect large numbers of macrophages in the setting of interstitial inflammation without depleting them. These observations point to the need for future investigations into mechanisms of CD4+ T cell depletion at this mucosal site, and into mechanisms by which macrophage populations are maintained despite high levels of infection. The large numbers of SIV RNA+ macrophages in lungs in the setting of interstitial inflammation indicates that lung macrophages can be an important source for SIV persistent infection.
College of Life Sciences, Nankai University, Tianjin, People's Republic of China; Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, United States of America.
Yue
Y
Li
Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, United States of America.
Guobin
G
Kang
Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Lijie
L
Duan
Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, United States of America.
Wuxun
W
Lu
Washington National Primate Research Center, Seattle, Washington, United States of America; Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington, United States of America.
Michael G
MG
Katze
BIOQUAL, Inc., 9600 Medical Center Drive, Rockville, Maryland, United States of America.
Mark G
MG
Lewis
Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.
Ashley T
AT
Haase
Nebraska Center for Virology, School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, United States of America.
Qingsheng
Q
Li
D000818:Animals; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology* / Q000821:virology; D057131:Immune Evasion; D007150:Immunohistochemistry; D008168:Lung / Q000276:immunology / Q000473:pathology* / Q000821:virology; D008212:Lymphocyte Depletion; D008253:Macaca mulatta; D016676:Macrophages, Alveolar / Q000276:immunology / Q000473:pathology* / Q000821:virology; D012367:RNA, Viral / Q000276:immunology*; D016097:Simian Acquired Immunodeficiency Syndrome / Q000276:immunology / Q000473:pathology* / Q000821:virology; D015302:Simian Immunodeficiency Virus / Q000276:immunology* / Q000472:pathogenicity; D013997:Time Factors; D019562:Viral Load
D012367:RNA, Viral