#hiv-1 — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #hiv-1, aggregated by home.social.
-
https://www.europesays.com/ie/317962/ Single-dose HIV vaccine candidate induces neutralizing antibodies #Antibodies #cancer #Éire #Glycan #HIV #HIV1 #IE #Immunization #Immunology #immunotherapy #Ireland #pH #Protein #Research #Science #Vaccine #virus
-
That Magic Gene…
While writing yesterday’s post about the evolution of languages, and the importance of genetic information in reconstructing the story thereof, I was reminded of a post I wrote a while ago about the peculiarities of my own genome, a listing of which I have on a CD-ROM at home. There’s not as much data involved as you might think: it’s effectively only about 800 MB.
Anyway, to cut a long story short, it turns out that I have the CCR5-Δ32 genetic mutation. Not only that, I have it twice over, in that I have two copies (homozygotes). I must therefore have inherited it from both parents. This mutation confers virtually complete immunity from HIV-1 infection.
The above graphic shows that more than 10% of the population in Northern Europe has this mutation in just one allele (i.e. they are heterozygotic). To get an estimate of how many have the form on two alleles (i.e. homozygotic) form you can just square that number, so around 1% or more.
It is thought that the CCR5-Δ32 mutation occurred in a single individual in Scandinavia around 1,000 years ago. When I wrote that post I tacitly assumed that it had propagated passively, i.e. without any particular selection, to the modern era. That it reached 10% of the population starting from just one individual surprised me, but I let it pass.
More recently, I came across a paper about how advances in genetics have impacted epidemiological studies. In the abstract it shows that my assumption was probably incorrect.
Algorithms of molecular evolutionary theory suggested that the CCR5-Δ32 mutation occurred but once in the last millennium and rose by strong selective pressure relatively recently to a ~10% allele frequency in Europeans.
It goes on to say this:
Several lines of evidence support the hypothesis that CCR5-Δ32 was selected due to its protective influence to resist Yersinia pestis, the agent of the Black Death/bubonic plague of the 14th century.
I didn’t mention in yesterday’s post that evidence of the plague bacillus is found in a significant number of prehistoric human remains and this almost certainly played a role in the ebb and flow of populations. In the context of CCR5-∆32, however it seems that it may have been advantageous to carry it long before the arrival of HIV/AIDS. That might account for it reaching the relatively high level that it did.
Among the downsides, however, as the article explains, are an increased risk for encephalomyelitis and death when infected with the West Nile virus. Hopefully further cohort studies of people with this mutation will help elucidate its effect on other diseases.
By the way, in contrast to most people I know, I have still never had Covid-19…
-
That Magic Gene…
While writing yesterday’s post about the evolution of languages, and the importance of genetic information in reconstructing the story thereof, I was reminded of a post I wrote a while ago about the peculiarities of my own genome, a listing of which I have on a CD-ROM at home. There’s not as much data involved as you might think: it’s effectively only about 800 MB.
Anyway, to cut a long story short, it turns out that I have the CCR5-Δ32 genetic mutation. Not only that, I have it twice over, in that I have two copies (homozygotes). I must therefore have inherited it from both parents. This mutation confers virtually complete immunity from HIV-1 infection.
The above graphic shows that more than 10% of the population in Northern Europe has this mutation in just one allele (i.e. they are heterozygotic). To get an estimate of how many have the form on two alleles (i.e. homozygotic) form you can just square that number, so around 1% or more.
It is thought that the CCR5-Δ32 mutation occurred in a single individual in Scandinavia around 1,000 years ago. When I wrote that post I tacitly assumed that it had propagated passively, i.e. without any particular selection, to the modern era. That it reached 10% of the population starting from just one individual surprised me, but I let it pass.
More recently, I came across a paper about how advances in genetics have impacted epidemiological studies. In the abstract it shows that my assumption was probably incorrect.
Algorithms of molecular evolutionary theory suggested that the CCR5-Δ32 mutation occurred but once in the last millennium and rose by strong selective pressure relatively recently to a ~10% allele frequency in Europeans.
It goes on to say this:
Several lines of evidence support the hypothesis that CCR5-Δ32 was selected due to its protective influence to resist Yersinia pestis, the agent of the Black Death/bubonic plague of the 14th century.
I didn’t mention in yesterday’s post that evidence of the plague bacillus is found in a significant number of prehistoric human remains and this almost certainly played a role in the ebb and flow of populations. In the context of CCR5-∆32, however it seems that it may have been advantageous to carry it long before the arrival of HIV/AIDS. That might account for it reaching the relatively high level that it did.
Among the downsides, however, as the article explains, are an increased risk for encephalomyelitis and death when infected with the West Nile virus. Hopefully further cohort studies of people with this mutation will help elucidate its effect on other diseases.
By the way, in contrast to most people I know, I have still never had Covid-19…
-
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology https://plos.io/45VTGBR
-
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology https://plos.io/45VTGBR
-
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology https://plos.io/45VTGBR
-
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology https://plos.io/45VTGBR
-
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @PLOSBiology https://plos.io/45VTGBR
-
Aquarius helicase facilitates HIV-1 integration into R-loop enriched genomic regions.
#HIV1 #HIV1Integration #Rloops #Integrase #Helicases #IntronBindingComplex
-
Aquarius helicase facilitates HIV-1 integration into R-loop enriched genomic regions.
#HIV1 #HIV1Integration #Rloops #Integrase #Helicases #IntronBindingComplex
-
SAMD9 & SAMD9L are restriction factors of #poxviruses, what about other #viruses? @Alexandre_Lgrnd @Lucie_Virevolte &co show that SAMD9L inhibits #HIV1 & other primate lentiviruses via a Schlafen-like active site, disrupting viral translation #PLOSBiology https://plos.io/4cn9ZZc
-
SAMD9 & SAMD9L are restriction factors of #poxviruses, what about other #viruses? @Alexandre_Lgrnd @Lucie_Virevolte &co show that SAMD9L inhibits #HIV1 & other primate lentiviruses via a Schlafen-like active site, disrupting viral translation #PLOSBiology https://plos.io/4cn9ZZc
-
SAMD9 & SAMD9L are restriction factors of #poxviruses, what about other #viruses? @Alexandre_Lgrnd @Lucie_Virevolte &co show that SAMD9L inhibits #HIV1 & other primate lentiviruses via a Schlafen-like active site, disrupting viral translation #PLOSBiology https://plos.io/4cn9ZZc
-
SAMD9 & SAMD9L are restriction factors of #poxviruses, what about other #viruses? @Alexandre_Lgrnd @Lucie_Virevolte &co show that SAMD9L inhibits #HIV1 & other primate lentiviruses via a Schlafen-like active site, disrupting viral translation #PLOSBiology https://plos.io/4cn9ZZc
-
SAMD9 & SAMD9L are restriction factors of #poxviruses, what about other #viruses? @Alexandre_Lgrnd @Lucie_Virevolte &co show that SAMD9L inhibits #HIV1 & other primate lentiviruses via a Schlafen-like active site, disrupting viral translation #PLOSBiology https://plos.io/4cn9ZZc
-
The #African #natural product #knipholone #anthrone and its analogue anthralin (dithranol) enhance #hiv1 latency reversal
-
The #African #natural product #knipholone #anthrone and its analogue anthralin (dithranol) enhance #hiv1 latency reversal
-
The #African #natural product #knipholone #anthrone and its analogue anthralin (dithranol) enhance #hiv1 latency reversal
-
The #African #natural product #knipholone #anthrone and its analogue anthralin (dithranol) enhance #hiv1 latency reversal
-
The #African #natural product #knipholone #anthrone and its analogue anthralin (dithranol) enhance #hiv1 latency reversal
-
Transcriptional and #chromatin profiling of human blood innate #lymphoid cell subsets sheds light on #HIV1 pathogenesis
Luban Lab and collaborators
https://www.embopress.org/doi/full/10.15252/embj.2023114153 -
Transcriptional and #chromatin profiling of human blood innate #lymphoid cell subsets sheds light on #HIV1 pathogenesis
Luban Lab and collaborators
https://www.embopress.org/doi/full/10.15252/embj.2023114153 -
Transcriptional and #chromatin profiling of human blood innate #lymphoid cell subsets sheds light on #HIV1 pathogenesis
Luban Lab and collaborators
https://www.embopress.org/doi/full/10.15252/embj.2023114153 -
Transcriptional and #chromatin profiling of human blood innate #lymphoid cell subsets sheds light on #HIV1 pathogenesis
Luban Lab and collaborators
https://www.embopress.org/doi/full/10.15252/embj.2023114153 -
🧵 1/2
How long did it take us to discover that #HIV first infected humans half a century before western scientists noticed it?
As in the current dominant #HIV1 strain first went from chimps to humans in about the #1920s
There's been multiple #spillover events from multiple species, so this has probably been happening for 1000s of years? (but older #spillovers didn't get far because it's not very contagious)
tweeted https://twitter.com/evolving_string/status/1635681501965864960
-
🧵 1/2
How long did it take us to discover that #HIV first infected humans half a century before western scientists noticed it?
As in the current dominant #HIV1 strain first went from chimps to humans in about the #1920s
There's been multiple #spillover events from multiple species, so this has probably been happening for 1000s of years? (but older #spillovers didn't get far because it's not very contagious)
tweeted https://twitter.com/evolving_string/status/1635681501965864960
-
#covid19
L’étrange #coronavirus mutant de Wuhan pose question – medias-presse.infoIl contiendrait des inserts du virus du #sida #HIV1 selon des analyses génétiques indiennes. #biorxiv_bioinfo
https://www.medias-presse.info/letrange-coronavirus-mutant-de-wuhan-pose-question/117362/
-
#covid19
L’étrange #coronavirus mutant de Wuhan pose question – medias-presse.infoIl contiendrait des inserts du virus du #sida #HIV1 selon des analyses génétiques indiennes. #biorxiv_bioinfo
https://www.medias-presse.info/letrange-coronavirus-mutant-de-wuhan-pose-question/117362/