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What are the natural immune factors in the human body that can inhibit HIV replication

  After human acquired immunodeficiency virus type 1 (HIV-1) infects the human body, some host cell proteins inhibit HIV-1 at different stages of its life cycle. Identifying novel host restriction factors and elucidating their mechanism of action may be helpful for the future of AIDS. provide ideas for the development of treatments and vaccines. Common host restriction factors are as follows.
1. APOBEC3G (A3G)

  A3G can be packaged into virus particles and play an antiviral role in the reverse transcription process of the virus. It can deaminate adenine or cytosine on the negative strand of new bovine DNA to xanthine or uracil, resulting in a C→A hypermutation that is lethal to the virus, while APOBEC3G can be antagonized by the Vif protein of HIV-1.
2. SAMHD1

  Expressed in dendritic and myeloid cells, reduces dNTP levels by affecting phosphohydrolase activity and interferes with HIV replication. And has nuclease activity to degrade viral RNA. SAMHD1 can be antagonized by Vpx and Vpr.
3. Tetherin

  It is a host restriction factor induced by interferon alpha, which can bind nascent HIV virus particles to the cell surface and prevent virus release. Vpu antagonizes the function of Tetherin and is an important virulence factor for HIV-1 to complete cross-species transmission.
4. Translocator protein (TSPO)

  TSPO located on the mitochondrial membrane can interact with VDAC on the mitochondria-associated ER membrane to change the membrane potential and block the release of reactive oxygen species to reduce the oxidative state in the endoplasmic reticulum, leading to Env misfolding and recognition through the ERAD pathway for degradation, and ultimately The nascent HIV-1 virus is Env-deficient and less infectious.
5. Endoplasmic reticulum mannosidase I (endoplas-mic reticulumal, 2-mannosidase I, ER-MAN I)

  High expression of ERMan I in the endoplasmic reticulum increases the expression of mitochondrial TSPO, disrupts the optimal oxidative state necessary for proper folding of Env in the endoplasmic reticulum, and misfolds Env, ultimately leading to its degradation.
6. Guanylate-binding protein 5 (guanylate-binding protein 5, GBP5)

  CBP5, a member of the interferon-induced guanosine triphosphatase (CTPascs) superfamily, has been shown to affect HIV-1 envelope by interfering with N-linked oligosaccharide glycosylation of envelope glycoproteins in the Golgi Gading of glycoproteins increases immature gp160 on the envelope of progeny viruses and reduces HIV-1 infectivity.
7. Serine incor-porator (serine incor-porator, SERINC3/5)

  In the absence of the negative regulator Nef of HIV-1 or the overexpression of SERINC5 itself, SERINC5 can bind to its progeny viral envelope with high affinity, thereby inhibiting the formation of small fusion pores between HIV-1 and host cells , thereby limiting the fusion of HIV-1 with host cells and ultimately reducing the infectivity of HIV-1. The SERINC protein may also interact with the Env protein of HIV-1, causing a conformational change in the Env protein, slowing down the fusion process of HIV-1 with the host cell, and exposing HIV-1 to the surface that can bind to various neutralizing antibodies. , thereby inhibiting the replication of HIV-1.
8. Zinc-fin-ger antiviral protein (ZAP)

  ZAP overexpression inhibits HIV-1 replication by preventing HIV-1 mRNA translation. The mechanism may be: (1) ZAP binds to host cell eIF4G, so that viral mRNA cannot be successfully translated; (2) ZAP can bind to viral mRNA, bind to ZAP-binding response element (ZRE) or indirectly affect RNA helicase. p72/DDX17 recruits substances with mRNA-degrading enzymatic activity to degrade viral mRNA.
9.TRAB domain-containing protein 2A (TRAB domain-containing protein2A, TRABD2A)

  Members of this protein family mainly include TRABD2A and TRABD2B. TRABD2A is mainly expressed on the surface of resting CD4+ T cells. TRABD2A can play an antiviral function in HIV-1 infection. It degrades the viral structural protein Gag on the CD4+ T cell membrane to limit HIV-1 in resting CD4+ T cells. Progeny assembly, which in turn inhibits HIV-1 replication.
  The identification of host restriction factors is still a hot spot in the study of anti-HIV innate immunity. Scientists continue to discover anti-HIV natural restriction factors, which provide a potential strategy for understanding the mechanism of HIV cross-species transmission and developing new anti-HIV/AIDS therapies. .

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