Abstract
Despite over 30 years of research, the contribution of type I interferons (IFN-Is) to both the control of HIV replication and initiation of immunologic damage remains debated. In acute infection, IFN-Is, likely from plasmacytoid dendritic cells (pDCs), activate NK cells and upregulate restriction factors targeting virtually the entire HIV life cycle. In chronic infection, IFN-Is may also contribute to CD4 T cell loss and immune exhaustion. pDCs subsequently infiltrate lymphoid and mucosal tissues, and their circulating populations wane in chronic infection; IFN-I may be produced by other cells. Data from nonhuman primates indicate prompt IFN-I signaling is critical in acute infection. Whereas some studies showed IFN-I administration without combination antiretroviral therapy (cART) is beneficial, others suggest that stimulating or blocking IFN-I signaling in chronic ART-suppressed HIV infection has had positive results. Here, we describe the history of HIV and IFN-I, IFN-I’s sources, IFN-I’s effects on HIV control and host defense, and recent interventional studies in SIV and HIV infection.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 41-53 |
| Number of pages | 13 |
| Journal | Current HIV/AIDS Reports |
| Volume | 12 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2015 |
Fingerprint
Keywords
- Acute HIV infection
- Chronic HIV infection
- HIV
- IFN
- ISG
- SIV
- Type I interferon
ASJC Scopus subject areas
- Virology
- Infectious Diseases
Cite this
Type I Interferon : Understanding Its Role in HIV Pathogenesis and Therapy. / Bosinger, Steven E.; Utay, Netanya S.
In: Current HIV/AIDS Reports, Vol. 12, No. 1, 2015, p. 41-53.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Type I Interferon
T2 - Understanding Its Role in HIV Pathogenesis and Therapy
AU - Bosinger, Steven E.
AU - Utay, Netanya S.
PY - 2015
Y1 - 2015
N2 - Despite over 30 years of research, the contribution of type I interferons (IFN-Is) to both the control of HIV replication and initiation of immunologic damage remains debated. In acute infection, IFN-Is, likely from plasmacytoid dendritic cells (pDCs), activate NK cells and upregulate restriction factors targeting virtually the entire HIV life cycle. In chronic infection, IFN-Is may also contribute to CD4 T cell loss and immune exhaustion. pDCs subsequently infiltrate lymphoid and mucosal tissues, and their circulating populations wane in chronic infection; IFN-I may be produced by other cells. Data from nonhuman primates indicate prompt IFN-I signaling is critical in acute infection. Whereas some studies showed IFN-I administration without combination antiretroviral therapy (cART) is beneficial, others suggest that stimulating or blocking IFN-I signaling in chronic ART-suppressed HIV infection has had positive results. Here, we describe the history of HIV and IFN-I, IFN-I’s sources, IFN-I’s effects on HIV control and host defense, and recent interventional studies in SIV and HIV infection.
AB - Despite over 30 years of research, the contribution of type I interferons (IFN-Is) to both the control of HIV replication and initiation of immunologic damage remains debated. In acute infection, IFN-Is, likely from plasmacytoid dendritic cells (pDCs), activate NK cells and upregulate restriction factors targeting virtually the entire HIV life cycle. In chronic infection, IFN-Is may also contribute to CD4 T cell loss and immune exhaustion. pDCs subsequently infiltrate lymphoid and mucosal tissues, and their circulating populations wane in chronic infection; IFN-I may be produced by other cells. Data from nonhuman primates indicate prompt IFN-I signaling is critical in acute infection. Whereas some studies showed IFN-I administration without combination antiretroviral therapy (cART) is beneficial, others suggest that stimulating or blocking IFN-I signaling in chronic ART-suppressed HIV infection has had positive results. Here, we describe the history of HIV and IFN-I, IFN-I’s sources, IFN-I’s effects on HIV control and host defense, and recent interventional studies in SIV and HIV infection.
KW - Acute HIV infection
KW - Chronic HIV infection
KW - HIV
KW - IFN
KW - ISG
KW - SIV
KW - Type I interferon
UR - http://www.scopus.com/inward/record.url?scp=84925483168&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84925483168&partnerID=8YFLogxK
U2 - 10.1007/s11904-014-0244-6
DO - 10.1007/s11904-014-0244-6
M3 - Article
C2 - 25662992
AN - SCOPUS:84925483168
VL - 12
SP - 41
EP - 53
JO - Current HIV/AIDS Reports
JF - Current HIV/AIDS Reports
SN - 1548-3568
IS - 1
ER -