Another tool in the pandemic toolkit
The existential risks associated with global warming include coastal flooding, loss of fresh water, desertification, life-threatening temperatures and loss of ocean fisheries. Another risk is the spread of infectious diseases that are normally restricted to tropical latitudes. While the prospect of eliminating insect vectors such as Aedes and Anopheles mosquitoes, tsetse flies and triatomine bugs using CRISPR gene drives offers some hope, viruses and other parasites are notoriously resourceful and able to adapt to new hosts.
One of the lessons of the COVID-19 pandemic was how resourceful humans are in resisting behaviors that will protect themselves and others from infection, disability and death. Protection in the form of social distancing and vaccines was fervently resisted by people who preferred their personal beliefs over scientific data. “Herd immunity” was a panacea promoted by many. Yes, herd immunity worked to constrain the spread of the plague in the middle ages, but at the cost of a third to a half of the population, and when the next generation grew up, herd immunity disappeared and another epidemic ensued.
A recent proof-of-principle study offers another route to community protection that could bypass human superstition and selfishness. Real-time air monitoring in enclosed spaces (hospitals, restaurants, lecture and concert halls, indoor sports stadiums) could detect various respiratory viruses, including the SARS-CoV-2 virus that causes COVID-19, and trigger increased airflow or circulation to dilute and/or filter the pathogen to protect people without requiring masking, social distancing or vaccine certification.
“There is nothing at the moment that tells us how safe a room is,” Cirrito said. “If you are in a room with 100 people, you don’t want to find out five days later whether you could be sick or not. The idea with this device is that you can know essentially in real time, or every 5 minutes, if there is a live virus in the air.”
Read the rest here: Air monitor can detect COVID-19 virus variants in about five minutes
Assessing COVID Risk and More with Air Quality Monitors
Scientific American – October 13, 2021
Also,
Astronomy Tool Can Now Detect COVID in Breath
Scientific American -May 12, 2023
@Fred,
The Sci Am article on COVID risk is about using proxy markers. The report I posted is about actual real-time detection of virus.
Joel
question for you:
i was always told that American Indians were killed in great numbers by diseases that Europeans had acquired immunity to. I assumed wthout thinking about it that this meant that Europeans had acquired genetic immunity. But right now I can’t think of how that would work, absent simple die off of those genetically not immune. Care to help me understand this better?
The large variety of histocompatibility genes means that there is considerable variation in genetically linked vulnerability to many diseases. As a result, after many generations of exposure to zoonotic diseases from domesticated animals, Eurasian populations actually did have some genetic partial immunity; because the most vulnerable variants were systematically reduced.
@Rick,
The MHC is certainly mainly implicated, but apparently not the whole story.
“We identified 100 and 57 statistically significant windows for the LSBL/XP-EHH and LSBL/iHS analysis, respectively. Of these, three stood out as particularly compelling with respect to immune adaptation. The first was a 4 MB region located on chromosome 3 (chr3:12,300,001− 12,700,001) containing the gene PPARG, or Peroxisome Proliferator-Activated Receptor Gamma. It is a ligand-activated transcription factor that contributes to gene regulation as part of the PPAR-γ signaling pathway, which regulates lipid and glucose metabolism through the expression of cytokines and chemokines (Le Menn and Neels 2018). Importantly, the PPAR-γ signaling pathway activates both pro- and anti-inflammatory macrophages (Chawla 2010). The second was a region on chromosome 5 containing the gene GALNT10. GALNT10 interacts with MHC complex genes as well as various interleukin cytokines (Kakoola et al. 2014) and is responsible for regulating CD4+ T cells infiltration of macrophages and decreasing granzyme B expression in CD8+ T cells (Zhang et al. 2020). CD4+ T cells are crucial to immune memory and CD8+ T cells are essential for protection against viruses, intracellular bacterial infection, and tumor cells (Worthington et al. 2012). It should be cautioned, given the continuous legacy of infectious disease exposure in Mesoamerica, any gene(s) in this region could have been the target of past selection.
“The third compelling result included two related regions residing on separate chromosomes 6 and 16. The chromosome 6 result was anticipated given the presence of the MHC, a known region of high genomic diversity that contains 224 genes largely related to immunity (Trowsdale 1993; de Bakker et al. 2006). The MHC complex has been identified numerous times in natural selection scans performed in human populations and across other mammalian and aquatic species (Hughes and Yeager 1998b). We hypothesized that the haplotype, HLA-DPA1*01:03/DPB1*04:02, is most likely the target of selection given its primary role as a cell surface receptor in antigen-presenting cells—crucial to recognizing foreign pathogens. Hepatitis B (HB) may have driven selection on this haplotype across time given the continuous presence of pre- and post-colonial lineages of the virus. Both HLA-DPA1*01:03 and HLA-DPB1*04:02 alleles independently have been shown to be protective for HB infection and known to play a role in developing long-term seroprotective immunity following HB vaccination among East Asian populations (Chung et al. 2019; Ou et al. 2019, 2021; Wang et al. 2019, 2021; Sanchez-Mazas 2020). HB infection previously was thought to have originated in the Americas, but ancient DNA analysis has demonstrated that it most likely co-evolved with humans as we dispersed across the globe (Muhlemann et al. 2018). Therefore, lineages existing in the Americas and novel HB lineages introduced through European contact, in conjunction with shifting social demographics, likely shaped the HLA diversity among Indigenous American populations although uncertain to know for certain (Guzman-Solis et al. 2021). The second related region on chromosome 16 contained the genes, class II, major histocompatibility complex transactivator (CIITA), known to positively regulate chromosome 6 MHC Class II expression, and suppressor of cytokine signaling 1 (SOCS1) (Reith et al. 2005; Krawczyk and Reith 2006; Devaiah and Singer 2013). SOCS1 activation inhibits CIITA activation and therefore subsequent MHC Class II expression as part of the IFN-γ pathway (O’Keefe et al. 2001). We identified a cluster of SNPS exhibiting extreme LSBL values residing in the lincRNA, RP11-396B14.2. The gene targets of this lincRNA are currently unknown, but it lies immediately upstream of SOCS1. This provides evidence for natural selection acting on variation affecting transcription. Together, these two related windows on chromosomes 6 and 16 illustrate the potential importance of selection acting on complimentary regions.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10016042/
Joel
very impressive. but could you translate that for us ignorant folk. I was guessing that it might have been the virus that evolved…into less lethal forms, given their host genetics, for their own benefit, leaving the hosts (europeans) with immunity to the now non lethal forms (this would be “acquired” immunity for them, not inherited.)..(some risk i won’t be understood here. more risk that i could be completely wrong.) is what you are trying to say something like that?
Rick Shapiro
Same question.
I didn’t want to be a belittler here. I am sure the virus detectors will be a valuable tool. But masking, distancing, early detection, and sane response [read “The Premonition” for arguably insane responses on the part of our public health officials re Covid] will, I suspect, be more effective in limiting spread of future pandemics.