PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Stably expressed APOBEC3H forms a barrier for cross-species transmission of simian immunodeficiency virus of chimpanzee to humans.

Abstract APOBEC3s (A3s) are potent restriction factors of human immunodeficiency virus type 1/simian immunodeficiency viruses (HIV-1/SIV), and can repress cross-species transmissions of lentiviruses. HIV-1 originated from a zoonotic infection of SIV of chimpanzee (SIVcpz) to humans. However, the impact of human A3s on the replication of SIVcpz remains unclear. By using novel SIVcpz reporter viruses, we identified that human APOBEC3B (A3B) and APOBEC3H (A3H) haplotype II strongly reduced the infectivity of SIVcpz, because both of them are resistant to SIVcpz Vifs. We further demonstrated that human A3H inhibited SIVcpz by deaminase dependent as well independent mechanisms. In addition, other stably expressed human A3H haplotypes and splice variants showed strong antiviral activity against SIVcpz. Moreover, most SIV and HIV lineage Vif proteins could degrade chimpanzee A3H, but no Vifs from SIVcpz and SIV of gorilla (SIVgor) lineages antagonized human A3H haplotype II. Expression of human A3H hapII in human T cells efficiently blocked the spreading replication of SIVcpz. The spreading replication of SIVcpz was also restricted by stable A3H in human PBMCs. Thus, we speculate that stably expressed human A3H protects humans against the cross-species transmission of SIVcpz and that SIVcpz spillover to humans may have started in individuals that harbor haplotypes of unstable A3H proteins.
PMID
Related Publications

Analysis of human APOBEC3H haplotypes and anti-human immunodeficiency virus type 1 activity.

Transmission of simian immunodeficiency virus SIVcpz and the evolution of infection in the presence and absence of concurrent human immunodeficiency virus type 1 infection in chimpanzees.

The resistance of human APOBEC3H to HIV-1 NL4-3 molecular clone is determined by a single amino acid in Vif.

Neutralization properties of simian immunodeficiency viruses infecting chimpanzees and gorillas.

Recapitulating Cross-Species Transmission of Simian Immunodeficiency Virus SIVcpz to Humans by Using Humanized BLT Mice.

Authors

Mayor MeshTerms

Disease Transmission, Infectious

Simian Immunodeficiency Virus

Zoonoses

Keywords
Journal Title plos pathogens
Publication Year Start




PMID- 29267382
OWN - NLM
STAT- MEDLINE
DCOM- 20180102
LR  - 20180102
IS  - 1553-7374 (Electronic)
IS  - 1553-7366 (Linking)
VI  - 13
IP  - 12
DP  - 2017 Dec
TI  - Stably expressed APOBEC3H forms a barrier for cross-species transmission of
      simian immunodeficiency virus of chimpanzee to humans.
PG  - e1006746
LID - 10.1371/journal.ppat.1006746 [doi]
AB  - APOBEC3s (A3s) are potent restriction factors of human immunodeficiency virus
      type 1/simian immunodeficiency viruses (HIV-1/SIV), and can repress cross-species
      transmissions of lentiviruses. HIV-1 originated from a zoonotic infection of SIV 
      of chimpanzee (SIVcpz) to humans. However, the impact of human A3s on the
      replication of SIVcpz remains unclear. By using novel SIVcpz reporter viruses, we
      identified that human APOBEC3B (A3B) and APOBEC3H (A3H) haplotype II strongly
      reduced the infectivity of SIVcpz, because both of them are resistant to SIVcpz
      Vifs. We further demonstrated that human A3H inhibited SIVcpz by deaminase
      dependent as well independent mechanisms. In addition, other stably expressed
      human A3H haplotypes and splice variants showed strong antiviral activity against
      SIVcpz. Moreover, most SIV and HIV lineage Vif proteins could degrade chimpanzee 
      A3H, but no Vifs from SIVcpz and SIV of gorilla (SIVgor) lineages antagonized
      human A3H haplotype II. Expression of human A3H hapII in human T cells
      efficiently blocked the spreading replication of SIVcpz. The spreading
      replication of SIVcpz was also restricted by stable A3H in human PBMCs. Thus, we 
      speculate that stably expressed human A3H protects humans against the
      cross-species transmission of SIVcpz and that SIVcpz spillover to humans may have
      started in individuals that harbor haplotypes of unstable A3H proteins.
FAU - Zhang, Zeli
AU  - Zhang Z
AD  - Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty,
      Heinrich-Heine-Universitat Dusseldorf, Dusseldorf, Germany.
FAU - Gu, Qinyong
AU  - Gu Q
AD  - Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty,
      Heinrich-Heine-Universitat Dusseldorf, Dusseldorf, Germany.
FAU - de Manuel Montero, Marc
AU  - de Manuel Montero M
AUID- ORCID: 0000-0002-1245-0127
AD  - Institut Biologia Evolutiva (Universitat Pompeu Fabra/CSIC) ICREA, Barcelona,
      Spain.
FAU - Bravo, Ignacio G
AU  - Bravo IG
AUID- ORCID: 0000-0003-3389-3389
AD  - Laboratory MIVEGEC, UMR CNRS 5290, UM, Montpellier, France.
FAU - Marques-Bonet, Tomas
AU  - Marques-Bonet T
AD  - Institut Biologia Evolutiva (Universitat Pompeu Fabra/CSIC) ICREA, Barcelona,
      Spain.
FAU - Haussinger, Dieter
AU  - Haussinger D
AD  - Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty,
      Heinrich-Heine-Universitat Dusseldorf, Dusseldorf, Germany.
FAU - Munk, Carsten
AU  - Munk C
AUID- ORCID: 0000-0002-8026-9311
AD  - Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty,
      Heinrich-Heine-Universitat Dusseldorf, Dusseldorf, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171221
PL  - United States
TA  - PLoS Pathog
JT  - PLoS pathogens
JID - 101238921
RN  - EC 3.5.4.- (APOBEC3H protein, human)
RN  - EC 3.5.4.- (Aminohydrolases)
SB  - IM
MH  - Aminohydrolases/*metabolism
MH  - Animals
MH  - *Disease Transmission, Infectious
MH  - Humans
MH  - Pan troglodytes
MH  - Simian Acquired Immunodeficiency Syndrome/*transmission
MH  - *Simian Immunodeficiency Virus
MH  - *Zoonoses
EDAT- 2017/12/22 06:00
MHDA- 2018/01/03 06:00
CRDT- 2017/12/22 06:00
PHST- 2017/08/05 00:00 [received]
PHST- 2017/11/12 00:00 [accepted]
PHST- 2017/12/22 06:00 [entrez]
PHST- 2017/12/22 06:00 [pubmed]
PHST- 2018/01/03 06:00 [medline]
AID - 10.1371/journal.ppat.1006746 [doi]
AID - PPATHOGENS-D-17-01697 [pii]
PST - epublish
SO  - PLoS Pathog. 2017 Dec 21;13(12):e1006746. doi: 10.1371/journal.ppat.1006746.
      eCollection 2017 Dec.