PS2-52 Simian immunodeficiency virus infection in the brain leads to differential type i interferon signaling during acute infection

Cytokine ◽  
2010 ◽  
Vol 52 (1-2) ◽  
pp. 61
Author(s):  
Luna Alammar ◽  
Lucio Gama ◽  
Janice E. Clements
Keyword(s):  
Virus Infection ◽  
Simian Immunodeficiency Virus ◽  
Type I Interferon ◽  
Acute Infection ◽  
Simian Immunodeficiency Virus Infection ◽  
Type I ◽  
Interferon Signaling ◽  
Immunodeficiency Virus ◽  
Differential Type ◽  
The Brain

scholarly journals Modulation of Type I Interferon-Associated Viral Sensing during Acute Simian Immunodeficiency Virus Infection in African Green Monkeys

2014 ◽  
Vol 89 (1) ◽  
pp. 751-762 ◽  
Author(s):  
Simon P. Jochems ◽  
Gaël Petitjean ◽  
Désirée Kunkel ◽  
Anne-Sophie Liovat ◽  
Mickaël J. Ploquin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Simian Immunodeficiency Virus ◽  
Blood Cells ◽  
Type I Interferon ◽  
Acute Infection ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Immunodeficiency Virus ◽  
Siv Infection ◽  
Green Monkeys

ABSTRACTNatural hosts of simian immunodeficiency virus (SIV), such as African green monkeys (AGMs), do not progress to AIDS when infected with SIV. This is associated with an absence of a chronic type I interferon (IFN-I) signature. It is unclear how the IFN-I response is downmodulated in AGMs. We longitudinally assessed the capacity of AGM blood cells to produce IFN-I in response to SIV and herpes simplex virus (HSV) infection. Phenotypes and functions of plasmacytoid dendritic cells (pDCs) and other mononuclear blood cells were assessed by flow cytometry, and expression of viral sensors was measured by reverse transcription-PCR. pDCs displayed low BDCA-2, CD40, and HLA-DR expression levels during AGM acute SIV (SIVagm) infection. BDCA-2 was required for sensing of SIV, but not of HSV, by pDCs. In acute infection, AGM peripheral blood mononuclear cells (PBMCs) produced less IFN-I upon SIV stimulation. In the chronic phase, the production was normal, confirming that the lack of chronic inflammation is not due to a sensing defect of pDCs. In contrast to stimulation by SIV, more IFN-I was produced upon HSV stimulation of PBMCs isolated during acute infection, while the frequency of AGM pDCs producing IFN-I uponin vitrostimulation with HSV was diminished. Indeed, other cells started producing IFN-I. This increased viral sensing by non-pDCs was associated with an upregulation of Toll-like receptor 3 and IFN-γ-inducible protein 16 caused by IFN-I in acute SIVagm infection. Our results suggest that, as in pathogenic SIVmac infection, SIVagm infection mobilizes bone marrow precursor pDCs. Moreover, we show that SIV infection modifies the capacity of viral sensing in cells other than pDCs, which could drive IFN-I production in specific settings.IMPORTANCEThe effects of HIV/SIV infections on the capacity of plasmacytoid dendritic cells (pDCs) to produce IFN-Iin vivoare still incompletely defined. As IFN-I can restrict viral replication, contribute to inflammation, and influence immune responses, alteration of this capacity could impact the viral reservoir size. We observed that even in nonpathogenic SIV infection, the frequency of pDCs capable of efficiently sensing SIV and producing IFN-I was reduced during acute infection. We discovered that, concomitantly, cells other than pDCs had increased abilities for viral sensing. Our results suggest that pDC-produced IFN-I upregulates viral sensors in bystander cells, the latter gaining the capacity to produce IFN-I. These results indicate that in certain settings, cells other than pDCs can drive IFN-I-associated inflammation in SIV infection. This has important implications for the understanding of persistent inflammation and the establishment of viral reservoirs.

scholarly journals Highly Activated CD8+T Cells in the Brain Correlate with Early Central Nervous System Dysfunction in Simian Immunodeficiency Virus Infection

2001 ◽  
Vol 167 (9) ◽  
pp. 5429-5438 ◽  
Author(s):  
Maria Cecilia Garibaldi Marcondes ◽  
E. M. E. Burudi ◽  
Salvador Huitron-Resendiz ◽  
Manuel Sanchez-Alavez ◽  
Debbie Watry ◽  
...  
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Virus Infection ◽  
Simian Immunodeficiency Virus ◽  
Cd8 T Cells ◽  
Simian Immunodeficiency Virus Infection ◽  
Central Nervous System Dysfunction ◽  
Immunodeficiency Virus ◽  
The Brain

scholarly journals Nonpathogenesis of Simian Immunodeficiency Virus Infection Is Associated with Reduced Inflammation and Recruitment of Plasmacytoid Dendritic Cells to Lymph Nodes, Not to Lack of an Interferon Type I Response, during the Acute Phase

2009 ◽  
Vol 84 (4) ◽  
pp. 1838-1846 ◽  
Author(s):  
Laure Campillo-Gimenez ◽  
Mireille Laforge ◽  
Michèle Fay ◽  
Audrey Brussel ◽  
Marie-Christine Cumont ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Virus Infection ◽  
Lymph Nodes ◽  
Simian Immunodeficiency Virus ◽  
Rhesus Macaques ◽  
Plasmacytoid Dendritic Cells ◽  
Simian Immunodeficiency Virus Infection ◽  
Type I ◽  
Immunodeficiency Virus ◽  
Tlr9 Signaling

ABSTRACT Divergent Toll-like receptor 7 (TLR7) and TLR9 signaling has been proposed to distinguish pathogenic from nonpathogenic simian immunodeficiency virus infection in primate models. We demonstrate here that increased expression of type I interferon in pathogenic rhesus macaques compared to nonpathogenic African green monkeys was associated with the recruitment of plasmacytoid dendritic cells in the lymph nodes and the presence of an inflammatory environment early after infection, instead of a difference in the TLR7/9 response.

Interstitial pneumonia in simian immunodeficiency virus infection

1992 ◽  
Vol 167 (2) ◽  
pp. 241-247 ◽  
Author(s):  
A. Baskerville ◽  
A. D. Ramsay ◽  
B. J. Addis ◽  
M. J. Dennis ◽  
R. W. Cook ◽  
...  
Keyword(s):  
Virus Infection ◽  
Simian Immunodeficiency Virus ◽  
Interstitial Pneumonia ◽  
Simian Immunodeficiency Virus Infection ◽  
Immunodeficiency Virus
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