Biedrîba "Apvienîba HIV.LV" (ik dienu pl. 9 - 21)
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Jauna ìençtiska mutâcija un brînumaina rω-1 olbaltumviela no târpiem
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10.09.2019


Reta ìençtiska mutâcija, kas izraisa ekstremitâðu muskuïu distrofiju, aizsargâ no HIV, pavçstîjuði spâòu zinâtnieki.
Jauni sasniegumi mutâciju atklâðanâ, kas bûtu potenciâli noderîgas cîòâ ar HIV, parâdîjâs tikai 10 gadus pçc tam, kad slavenais “Berlînes pacients” izârstçjâs no HIV pçc donora, kuram bija gçna CCR5 mutâcija, kaulu smadzeòu transplantâcijas.
Spâòu zinâtnieku atklâtâ mutâcija attiecas uz gçnu TNPO3 un ir sastopama daudz retâk. To pirms daþiem gadiem konstatçja kâdas spâòu ìimenes locekïiem, kas cieta no ekstremitâðu muskuïu 1. tipa distrofijas.
Ârsti, izmeklçjuði ìimeni, noskaidroja, ka ðis gçns varçtu interesçt HIV pçtniekus, jo tam ir noteikta loma vîrusa pârneðanâ ðûnu iekðienç. (Lasiet zemâk oriìinâlrakstu angïu valodâ.)
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Antigçni, kurus satur ðistosomu olas, maina imûnsistçmas darbîbu, traucçjot tâs ðûnâm saistîties ar HIV daïiòâm. Turklât stimulç T-ðûnu augðanu, kas ir daudz noturîgâkas pret cilvçka imûndeficîta vîrusu. Pçtîjums publicçts þurnâlâ PLoS Pathogens.
Ðistosomas ir parazîtiskie plakani târpi, kas dzîvo asinîs un dçj olas cilvçka vçnâs. Ðistosomu olas spçj cînîties ar cilvçka imûnsistçmu, izdalot vielas, kas maina imûno atbildi. Galvenais mçríis, pret ko darbojas ðistosomu olu vielas, ir dendrîtu ðûnas. Vielas, ko izdala parazîti (rekombinanta olbaltumviela rω-1), saistâs ar dendrîta ðûnu receptoriem, traucçjot tiem normâli strâdât.
Dendrîtu ðûnas imûnsistçmai vajadzîgas tâpçc, lai T-ðûnas (T-limfocîtus) iepazîstinâtu ar iekïuvuðâs infekcijas antigçniem. Pçc tam, kad dendrîtu ðûnas atnesuðas limfmezglos antigçnus, aktivizçjas daþâdu tipu T-ðûnas, kas iznîcina organisma apdraudçjumu – patstâvîgi vai aktivizçjot B-ðûnas.
Parazîta aizsardzîba darbojas tikai pret to HIV veidu, kas izmanto CCR5 receptors, lai iekïûtu ðûnâ. HIV, kas izmanto CXCR4, neizjût nekâdu traucçjumu. Turklât pçtîjums tika veikts tikai ar HIV-1, bet ne HIV-2. (Lasiet zemâk oriìinâlrakstu angïu valodâ.)
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Source: MedicaExpress | «Researchers identify second gene mutation linked to HIV resistance» | https://medicalxpress.com/news/2019-08-mutation-rare-muscle-disease-hiv-.html
<... A rare genetic mutation that causes a form of muscular dystrophy affecting the limbs also protects against HIV infection. 
The breakthrough comes a decade after American Timothy Brown, known as the "Berlin Patient," became the first person cured of HIV after a bone marrow transplant from a donor with a mutation of the CCR5 gene.
The newly-discovered mutation concerns the Transportin 3 gene (TNPO3) and is far more rare.
It was identified several years ago among members of a family in Spain who were suffering from type 1F limb-girdle muscular dystrophy.
Doctors studying the family learned that HIV researchers were interested in the same gene because it plays a role in transporting the virus inside cells.
They then got in touch with geneticists in Madrid, who took blood samples from those family members and infected the blood with HIV—revealing a welcome surprise.
The lymphocytes—white blood cells that are an important part of the immune system—of people with the rare muscular illness were naturally resistant to HIV, it emerged.
"This helps us to understand much better the transport of the virus in the cell," Jose Alcami, a virologist at the Carlos III Health Institute and co-author of a paper published in US journal PLOS Pathogens on the subject, told AFP. ...>
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Source: PLOS Pathogens | «Schistosoma mansoni soluble egg antigen (SEA) and recombinant Omega-1 modulate induced CD4+ T-lymphocyte responses and HIV-1 infection in vitro» | https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007924 |
<... Abstract
Parasitic helminths evade, skew and dampen human immune responses through numerous mechanisms. Such effects will likely have consequences for HIV-1 transmission and disease progression. Here we analyzed the effects that soluble egg antigen (SEA) from Schistosoma mansoni had on modulating HIV-1 infection and cytokine/chemokine production in vitro. We determined that SEA, specifically through kappa-5, can potently bind to DC-SIGN and thereby blocks DC-SIGN mediated HIV-1 trans-infection (p<0.05) whilst not interfering with cis-infection. DCs exposed to SEA whilst maturing under Th2 promoting conditions, will upon co-culture with naïve T-cells induce a T-cell population that was less susceptible to HIV-1 R5 infection (p<0.05) compared to DCs unexposed to SEA, whereas HIV-1 X4 virus infection was unaffected. This was not observed for DCs exposed to SEA while maturing under Th1 or Th1/Th2 (Tmix) promoting conditions. All T-cell populations induced by SEA exposed DCs demonstrate a reduced capacity to produce IFN-γ and MIP-1β. The infection profile of T-cells infected with HIV-1 R5 was not associated with down-modulation of CCR5 cell surface expression. We further show that DCs maturing under Tmix conditions exposed to plant recombinant omega-1 protein (rω-1), which demonstrates similar functions to natural ω-1, induced T-cell populations that were less sensitive for HIV-1 R5 infection (p<0.05), but not for X4 virus infection. This inhibition associated again with a reduction in IFN-γ and MIP-1β expression, but additionally correlated with reduced CCR5 expression. We have shown that SEA parasite antigens and more specifically rω-1 can modulate HIV-1 infectivity with the potential to influence disease course in co-infected individuals. ...>




 
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