Biedrba "Apvienba HIV.LV" (ik dienu pl. 9 - 21)
apvieniba@apvienibahiv.lv

 
   
108076

Zintnieki terapijas laik pacienta organism atradui HIV slptuves
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23.09.2019


Beu zintnieki atkljui pacienta organism vietas, kur slpjas HIV rstanas kursa laik. Kad terapija tiek prtraukta, vruss iznk no slptuves un atkal nonk asins, izraisot slimbas saasinanos. Zintnieku ptjuma rezultti publicti urnl Cell Host and Microbe.
Paradoksli, bet imnnas, kurm ir jnomc HIV aktivitte, vienlaikus atbild par vrusu rezervuru veidoanos. Atkljuma svargkais aspekts ir tas, ka, novjinoties imunittei, vrusa izmeana notiek nevis no viena orgna vai organisma daas, bet no vism organisma sistmm.
T ka zintnieki ir iemcjuies kontrolt mirkli, kad vruss tiek iemests asins, tagad viiem ir vieglk noteikt rezervuru atraans vietas, atzmts ptjuma ziojum.
Iepriek grupa zintnieku no Kandas, veices, Lielbritnijas, Krievijas, ASV un Somijas atkljui mehnismu, kas HIV padara nekaitgu. Tas izpauas tdjdi, ka pretvrusa organiskie savienojumi, nonkot organism, izmazg cinku no vrusa molekulm un d veid dezaktiv to.
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Source: Cell Host and Microbe | HIV Rebound Is Predominantly Fueled by Genetically Identical Viral Expansions from Diverse Reservoirs | https://www.cell.com/cell-host-microbe/pdfExtended/S1931-3128(19)30368-3 |
<... Highlights

HIV-1 sequences sampled from different reservoirs were compared to rebound viruses in 11 individuals

Rebound viruses can originate from various cellular and anatomical compartments

Cellular proliferation is an important driver of HIV persistence

Cure strategies should take into account the lack of a prominent HIV rebound origin
Summary
Viral rebound upon stopping combined antiretroviral therapy poses a major barrier toward an HIV cure. Cellular and anatomical sources responsible for reinitiating viral replication remain a subject of ardent debate, despite extensive research efforts. To unravel the source of rebounding viruses, we conducted a large-scale HIV-STAR (HIV-1 sequencing before analytical treatment interruption to identify the anatomically relevant HIV reservoir) clinical trial. We collected samples from 11 participants and compared the genetic composition of (pro)viruses collected under treatment from different cellular and anatomical compartments with that of plasma viruses sampled during analytical treatment interruption. We found a remarkably heterogeneous source of viral rebound. In addition, irrespective of the compartment or cell subset, genetically identical viral expansions played a significant role in viral rebound. Our study suggests that although there does not seem to be a primary source for rebound HIV, cellular proliferation is an important driver of HIV persistence and should therefore be considered in future curative strategies. ....>




 
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