The Mu variant, also known as B.1.621, was added to the WHO’s watchlist on 30 August after it was detected in 39 countries and found to possess a cluster of mutations that may make it less susceptible to the immune protection many have acquired. According to the WHO’s weekly bulletin on the pandemic, the Mu variant “has a constellation of mutations that indicate potential properties of immune escape”. The Mu variant was first identified in Colombia in January 2021. At least 32 cases of the Mu variant have been detected in the UK, where the pattern of infections suggests it was brought in by travellers on multiple occasions.
https://www.theguardian.com/world/2021/sep/01/who-monitoring-new-coronavirus-variant-named-mu
A message on the r/Futurology forum said “people are dying from misinformation” related to coronavirus. “Futurology has gone private to protest Reddit’s inaction on Covid-19 misinformation,” the message said. “Weaponized misinformation is a key problem shaping our future. Reddit won’t enforce their policies against misinformation, brigading, and spamming.”
https://www.theguardian.com/technology/2021/sep/01/reddit-communities-go-dark-in-protest-over-covid-misinformation
Note To Reddit. Your Out.
Immunity to Pathogens and Tumors
Stephanie Jost, Marcus Altfeld, in Encyclopedia of Immunobiology, 2016
HIV-1 Escape from NKG2D-Mediated Recognition by NK Cells
HIV-1 infection does not only affect HLA class I expression, thereby impacting recognition by KIRs, but can also trigger the upregulation of ligands for less polymorphic receptors, such as NKG2D. Expression of these stress-induced ligands, and particularly that of UL16-binding proteins (ULBPs), results in increased recognition and killing of both HIV-1-infected and uninfected bystander CD4+ T cells by NK cells (Fogli et al., 2008; Norman et al., 2011; Richard et al., 2013; Ward et al., 2007). Given the high capacity of NKG2D ligands to activate NK cells, HIV-1, like other viruses, has evolved elaborate mechanisms to evade NKG2D-mediated recognition. For instance, the HIV-1 Nef protein appears to not only downregulate HLA-A and HLA-B molecules, but also to limit the expression of NKG2D ligands by triggering the degradation of ULBP-1 and -2, and to a lesser extent, that of MICA (Cerboni et al., 2007). An alternative way for HIV-1 to impair NKG2D-mediated NK cell activation might consist in promoting enzymatic cleavage of MICA and MICB from the surface of HIV-1-infected cells. Engagement of NKG2D by the soluble forms of MICA/B would lead to its downregulation, and to the generation of anergic NK cells. This hypothesis is supported by studies describing elevated plasma levels of soluble MICA and compromised NKG2D-mediated NK cell responses in chronic HIV-1 infection (Nolting et al., 2010), and would explain why MICA has been repeatedly reported to be barely detectable at the surface of CD4+ T cells following HIV-1 infection (Fogli et al., 2008; Ward et al., 2007). Overall, those strategies evolved by HIV-1 to escape from NKG2D recognition suggest that this pathway might play a significant role in the recognition of HIV-1-infected cells by NK cells.
https://www.sciencedirect.com/topics/medicine-and-dentistry/human-immunodeficiency-virus-1
SCIENCEINSIDERHEALTH
What does the Delta variant have in store for the United States? We asked coronavirus experts
Increased vaccination and a return to wearing masks could avert worst-case scenarios for the Delta-driven surge
No comments:
Post a Comment