Mouse serum factor(s) down-modulate the CD4 and CXCR4 molecules on human T cells conferring resistance to HIV infection in NOG mice

Human cells have developed innate immunity, exploiting several means to block virus infection, and viruses have evolved diverse strategies to resist these. We show here that the human immunodeficiency virus 1 (HIV-1) could neither progressively infect engrafted human leukemic T cells nor repress the...

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Bibliographic Details
Published in:Medical microbiology and immunology 2005-08, Vol.194 (4), p.175-180
Main Authors: ZAHIDUNNABI DEWAN, Md, TERASHIMA, Kazuo, AHMED, Sunjida, OHBA, Kenji, TARUISHI, Midori, YAMAMOTO, Naoki
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Biological Factors - physiology
Carrier Proteins
CD4 Antigens - metabolism
Cell Line, Transformed - immunology
Cell Line, Transformed - virology
Cells
Disease Models, Animal
Down-Regulation
Fundamental and applied biological sciences. Psychology
HIV
HIV Infections - immunology
HIV-1
Human immunodeficiency virus
Human immunodeficiency virus 1
Human viral diseases
Humans
Infectious diseases
Medical sciences
Mice
Mice, Inbred NOD
Mice, SCID
Microbiology
Miscellaneous
Molecules
Receptors, CXCR4 - metabolism
Rodents
Serum - physiology
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
T-Lymphocytes - virology
Tumors
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Virology
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Summary:Human cells have developed innate immunity, exploiting several means to block virus infection, and viruses have evolved diverse strategies to resist these. We show here that the human immunodeficiency virus 1 (HIV-1) could neither progressively infect engrafted human leukemic T cells nor repress their growth in NOG mice. However, ED-40515(-) cells infected with HIV-1 before inoculation were found to significantly delay the onset of tumor growth and increased the survival period of NOG mice. ED-40515(-) tumor cells showed resistance to HIV-1 which was apparently correlated with the down-regulation of CD4 and CXCR4 molecules in NOG mice. Serum from three different mouse strains, including NOG, retained a suppressive effect on the CD4 molecule of ED-40515(-) cells in vitro. ED-40515(-) cells obtained from mice re-expressed CD4 and CXCR4 molecules upon in vitro culture and were again successfully infected with HIV-1. These findings indicate that HIV-1 may initially successfully delay or regress tumor growth in NOG mice, but eventually fails to do so because of the evolution of HIV-resistant cells due to a rapid down-modulation of CD4 and CXCR4. Our data also demonstrated that some unknown soluble factor(s) present in mouse serum was responsible for conferring resistance to HIV infection to human T cells.
ISSN:0300-8584
1432-1831
DOI:10.1007/s00430-004-0234-1