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

 
   
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Jauna entiska mutcija un brnumaina rω-1 olbaltumviela no trpiem
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10.09.2019


Reta entiska mutcija, kas izraisa ekstremitu muskuu distrofiju, aizsarg no HIV, pavstjui spu zintnieki.
Jauni sasniegumi mutciju atklan, kas btu potencili nodergas c ar HIV, pardjs tikai 10 gadus pc tam, kad slavenais Berlnes pacients izrstjs no HIV pc donora, kuram bija gna CCR5 mutcija, kaulu smadzeu transplantcijas.
Spu zintnieku atklt mutcija attiecas uz gnu TNPO3 un ir sastopama daudz retk. To pirms daiem gadiem konstatja kdas spu imenes locekiem, kas cieta no ekstremitu muskuu 1. tipa distrofijas.
rsti, izmekljui imeni, noskaidroja, ka is gns vartu interest HIV ptniekus, jo tam ir noteikta loma vrusa prnean nu iekien. (Lasiet zemk oriinlrakstu angu valod.)
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Antigni, kurus satur istosomu olas, maina imnsistmas darbbu, traucjot ts nm saistties ar HIV daim. Turklt stimul T-nu auganu, kas ir daudz noturgkas pret cilvka imndeficta vrusu. Ptjums publicts urnl PLoS Pathogens.
istosomas ir paraztiskie plakani trpi, kas dzvo asins un dj olas cilvka vns. istosomu olas spj cnties ar cilvka imnsistmu, izdalot vielas, kas maina imno atbildi. Galvenais mris, pret ko darbojas istosomu olu vielas, ir dendrtu nas. Vielas, ko izdala parazti (rekombinanta olbaltumviela rω-1), saists ar dendrta nu receptoriem, traucjot tiem normli strdt.
Dendrtu nas imnsistmai vajadzgas tpc, lai T-nas (T-limfoctus) iepazstintu ar iekuvus infekcijas antigniem. Pc tam, kad dendrtu nas atnesuas limfmezglos antignus, aktivizjas dadu tipu T-nas, kas izncina organisma apdraudjumu  patstvgi vai aktivizjot B-nas.
Parazta aizsardzba darbojas tikai pret to HIV veidu, kas izmanto CCR5 receptors, lai iektu n. HIV, kas izmanto CXCR4, neizjt nekdu traucjumu. Turklt ptjums tika veikts tikai ar HIV-1, bet ne HIV-2. (Lasiet zemk oriinlrakstu angu valod.)
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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 HIVrevealing a welcome surprise.
The lymphocyteswhite blood cells that are an important part of the immune systemof 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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