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Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
Published on: January 7, 2019
Mice transgenic for simian immunodeficiency virus nef are immunologically compromised
N B Larsen1, H W Kestler, J J Docherty
1Department of Microbiology/Immunology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272, USA.
Journal of Biomedical Science
|August 6, 1998
Summary
The simian immunodeficiency virus (SIV) nef gene impairs immune responses. Mice with the SIV nef gene showed increased mortality and immune dysfunction when exposed to herpes simplex virus type-1 (HSV-1).
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- An intact nef gene is crucial for rapid immunodeficiency development in HIV and SIV infections.
- The specific role of nef in modulating the host immune response remains incompletely understood.
Purpose of the Study:
- To investigate the impact of the simian immunodeficiency virus (SIV) nef gene on the humoral and cellular immune response.
- To assess the role of nef in immune dysfunction using a murine model.
Main Methods:
- Generation of mice transgenic for SIVmac239 nef.
- Challenge of transgenic and control mice with herpes simplex virus type-1 (HSV-1).
- Measurement of humoral immune responses (IgG subclass titers, neutralizing antibody titers) and cellular immune responses (T cell proliferation to PHA).
Main Results:
- Mice transgenic for SIV nef exhibited increased mortality rates following HSV-1 challenge.
- Altered antibody kinetics were observed, with rising IgG subclass titers in nef+ mice and decreasing titers in nef- mice over 32 weeks.
- nef- mice showed a greater increase in HSV-neutralizing antibodies after secondary challenge compared to nef+ mice.
- A decreased proliferative response to PHA was noted in T cells from nef+ animals.
Conclusions:
- The presence of the SIV nef gene is sufficient to induce immune dysfunction in a murine model.
- Nef appears to play a significant role in modulating both humoral and cellular immune responses, potentially contributing to increased susceptibility to secondary infections.
