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Good articleHIV has been listed as one of the Natural sciences good articles under the good article criteria. If you can improve it further, please do so. If it no longer meets these criteria, you can reassess it.
In the news Article milestones
DateProcessResult
September 18, 2005Peer reviewReviewed
December 23, 2005Good article nomineeListed
July 10, 2006Peer reviewReviewed
September 26, 2006Featured article candidateNot promoted
March 19, 2008Featured article candidateNot promoted
August 4, 2009Good article reassessmentKept
In the news A news item involving this article was featured on Wikipedia's Main Page in the "In the news" column on August 5, 2024.
Current status: Good article

RBCs are 100,000x larger than an HIV particle, not 60x.

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The diameter of a red blood cell is ~60x larger than the diameter of an HIV virion. Because volume scales as 4/3*pi*r^3, a red blood cell is in fact ~113,000x larger than an HIV virion. As worded now, this part at the head of the structure & genome section is highly misleading, since most people think about size of 3d objects in terms of volume not diameter. 165.124.224.110 (talk) 19:39, 7 April 2022 (UTC)[reply]

I agree, it is misleading. I will see what can be done. Thank you. Graham Beards (talk) 08:49, 8 April 2022 (UTC)[reply]

Updating References

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Hi, new user so apologies if this is in the wrong place. I noticed reference 15 has a broken link. As it happens, the ICTV has also released an updated version of the database (however, the taxonomy for HIV remains unchanged). The new link can be found here

Thanks, SuperiorPlot (talk) 18:53, 23 June 2022 (UTC)[reply]

Survival strategy

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"A survival strategy for any infectious agent is not to kill its host, but ultimately become a commensal organism."

Proof missing. How can a virus without a brain formulate a strategy? Based on which information received from whom? Then how does the virus project future events and devise counter measures? 194.207.180.128 (talk) 05:35, 28 September 2023 (UTC)[reply]

Arv

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what are the danger of avr is you overdoses Mantoa mollo (talk) 04:59, 2 October 2023 (UTC)[reply]

Semi-protected edit request on 16 April 2024

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"ADD under replication cycle section"

Viral Reservoir Survival and Clonal Expansion

Although antiretroviral therapy (ART) has been an effective measure to lower viral loads in the plasma to undetectable levels, integrated proviral sequences in CD4+ T cells will still be present in infected cells and continue to produce viral particles even after treatment [1]. This is why most individuals with HIV will need to continue being on ART even after viral loads are initially suppressed. Upon interruption of ART, individuals with HIV often experience a rebound of HIV virions. [2] The replication and persistence of HIV can be observed using three models: the active viral replications stage, prolonged survival and clonal expansion.

In active viral replication, an infected CD4+ T cell produces new viral particles which infects other CD4+ T cells. Upon usage of ART, the CD4+ T cell may not be able to produce new viral particles but will have been primed for survival due to upregulation of anti-apoptotic genes and downregulation of pro-apoptotic genes. [3] This allows the infected cell to survive and become a persistent viral reservoir. When infected CD4+ T cells replicate, they replicate the integrated HIV sequence along with its genome, leading to a process known as clonal expansion where the viral reservoir increases through the expansion of the infected clone.[4]

Producer and Nonproducer Proviruses which can lead to nonsuppressible viremia

Producer proviral sequences are often defined as integrated HIV sequences that can produce infectious particles, whereas nonproducer sequences show no evidence in being able to produce complete virions in the plasma.[5]

There is a higher frequency of producer proviral sequences integrated in chromosome 19.[6] Although the integration of HIV is thought to be relatively random process, different integration sites may differentiate whether a provirus becomes a producer or nonproducer.

There has been evidence to show that producer proviruses are often seen in highly transcribed sites leading to a higher transcription rate, compared to nonproducer proviruses which are more often seen in less transcribed regions of the chromosome.[7] Producer proviruses are also more observed to be in regions with higher number of H3K36me3 histones, which are associated with more permissively transcribed chromatin.[8] This may explain why most of plasma virions detected match the producer provirus. Nonproducer proviruses are also associated with large deletions and non-intact reservoirs which may prevent the complete transcription of HIV viral components.[9]

Regulation of Apoptotic Genes for Reservoir Survival

Non-Suppressible Viremia (NSV) is often described when an individual is on ART but cannot suppress their viral loads and continuously observes low, detectable viremia. Several factors may contribute to this condition including prolonged clonal expansion and regulated immune responses. CD4+ T cells infected with HIV may sometimes become more primed for survival through the downregulation of pro-apoptotic genes such as TNFRSF14 and the upregulation of anti-apoptotic genes such as MTRNR2L2, OPA1 and STK24.[10] The regulation of apoptotic genes promotes the survival of HIV-infected cells and protect cells from cytotoxic T cell responses.[11] NSV has also been associated with a downregulation of IFN signaling which are important inflammatory responses for the immune system.[12] When compared to individuals who are ART-suppressed, individuals with NSV often show decreased transcripts for IRF3, IRF7 and OAS1 which are important genes for host immune responses.[13] With the mediation of different antiviral and immune pathways, HIV-infected cells in NSV can continue to survive and produce virions. Shkim19 (talk) 06:24, 16 April 2024 (UTC)[reply]

References

  1. ^ Bongiovanni, Marco et al. “Treatment interruptions in HIV-infected subjects.” The Journal of antimicrobial chemotherapy vol. 58,3 (2006): 502-5. doi:10.1093/jac/dkl268
  2. ^ Li, Jonathan Z et al. “The size of the expressed HIV reservoir predicts timing of viral rebound after treatment interruption.” AIDS (London, England) vol. 30,3 (2016): 343-53. doi:10.1097/QAD.0000000000000953
  3. ^ Mohammadi, A., Etemad, B., Zhang, X. et al. Viral and host mediators of non-suppressible HIV-1 viremia. Nat Med 29, 3212–3223 (2023). https://doi.org/10.1038/s41591-023-02611-1
  4. ^ Halvas, E. K. et al. HIV-1 viremia not suppressible by antiretroviral therapy can originate from large T cell clones producing infectiousvirus.J.Clin.Invest.130,5847–5857(2020).
  5. ^ Mohammadi, A., Etemad, B., Zhang, X. et al. Viral and host mediators of non-suppressible HIV-1 viremia. Nat Med 29, 3212–3223 (2023). https://doi.org/10.1038/s41591-023-02611-1
  6. ^ Mohammadi, A., Etemad, B., Zhang, X. et al. Viral and host mediators of non-suppressible HIV-1 viremia. Nat Med 29, 3212–3223 (2023). https://doi.org/10.1038/s41591-023-02611-1
  7. ^ Vansant, Gerlinde et al. “The chromatin landscape at the HIV-1 provirus integration site determines viral expression.” Nucleic acids research vol. 48,14 (2020): 7801-7817. doi:10.1093/nar/gkaa536
  8. ^ Vansant, Gerlinde et al. “The chromatin landscape at the HIV-1 provirus integration site determines viral expression.” Nucleic acids research vol. 48,14 (2020): 7801-7817. doi:10.1093/nar/gkaa536
  9. ^ Einkauf, Kevin B et al. “Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses.” Cell vol. 185,2 (2022): 266-282.e15. doi:10.1016/j.cell.2021.12.011
  10. ^ Mohammadi, A., Etemad, B., Zhang, X. et al. Viral and host mediators of non-suppressible HIV-1 viremia. Nat Med 29, 3212–3223 (2023). https://doi.org/10.1038/s41591-023-02611-1
  11. ^ Ren, Yanqin et al. “BCL-2 antagonism sensitizes cytotoxic T cell-resistant HIV reservoirs to elimination ex vivo.” The Journal of clinical investigation vol. 130,5 (2020): 2542-2559. doi:10.1172/JCI132374
  12. ^ Rout, Saurav S et al. “Distinct effects of treatment with two different interferon-alpha subtypes on HIV-1-associated T-cell activation and dysfunction in humanized mice.” AIDS (London, England) vol. 36,3 (2022): 325-336. doi:10.1097/QAD.0000000000003111
  13. ^ Doehle, Brian P et al. “Human immunodeficiency virus type 1 mediates global disruption of innate antiviral signaling and immune defenses within infected cells.” Journal of virology vol. 83,20 (2009): 10395-405. doi:10.1128/JVI.00849-09
 Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format and provide a reliable source if appropriate. '''[[User:CanonNi]]''' (talk|contribs) 06:33, 16 April 2024 (UTC)[reply]
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