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New Hampshire House speaker dies of COVID-19 a week after swearing in

New Hampshire House speaker dies of COVID-19 a week after swearing in

New Hampshire Speaker of the House Richard ’Dick’ Hinch has died from Covid-19. Hinch, 71, had been elected to the post on Dec. 2. He previously served as New Hampshire’s House Republican leader from 2018 to 2020 and as House majority leader from 2015 to 2018. State Rep. Sherman Packard has been named acting speaker.

Kathy
Kathy
Chris
Chris 2 months

RIP Just sad that this has become such a partisan issue. Masks Vs No Masks. Republican Vs Democrats. Instead of actually seeing 300K people have died. And the numbers ticking.

porcus
porcus 2 months

Summary: The immune system is incredibly complex and decentralized; that's the whole point of it, to be able to respond to any invasion, any threat, anywhere in the body. There is A LOT of information out there, and trying to condense the underlying basis of the immune system into a NV comment just is not feasible; I'm going to outline the information that is known in the severe cases, only. The implications thus far are that those with severe or fatal COVID19 have defective immune systems, lacking certain immunological features and/or entering into an inflammation cascade. There are still a lot of questions remaining as to what the cause of the COVID19 deaths and severe causes are, but at this point this is what is known: SEVERE+: - low levels of interferons in the blood - high levels of interferons in the lungs (IL-6, IL-8, and TNF-a) - high levels of inflammatory immune response (this is bad, and can cause the immune system to attack healthy cells) - some patients appear to be less capable of producing an interferon response - severe cases have a strong correlation to the severity of the disease with the following interferons: IL-6, IL-10, and IP-10 - heightened immune activity present in those who had the severe form of the disease, present even after recovery - some severely ill patients have malfunctioning immune systems that recruit cells and proteins typically associated with parasitic worms, fungi, and bacteria instead of the virus itself. This implies a confused immune system in these patients - dysfunction in the anti-viral rapid-response immune cells (myeloid cells such as neutrophils and monocytes). German study of patients with the severe disease found that these cells seemed to be only partially activated, largely immature, and lacked critical surface proteins needed for presenting viral material to T cells. This implies that the severe patients had a dysfunctional immune system, as these features were not present in less severe cases - some researchers posit that COVID19 is a dangerous loop of ineffective immune system responses combined with continuous tissue inflammation - a myleoid triggered disease - immune response in the lungs is excessive inflammation and cytokine production. Immune response in the blood is the opposite - no cytokine production and suppression of inflammation (in sepsis, this is called immunoparalysis). Patients with moderate cases of COVID19 had less suppression in the blood - other immune system changes in the severe form of COVID19 include the alteration of NK (natural killer) cells; in moderate cases these NK cells are less differentiated and more focused on proliferating and secreting cytokines. In severe cases the NK cells are highly differentiated and target the virally infected cells and kill them. It is unknown at this time if the difference is due to the severity of the disease (necessitating such a response) or if it is due to a defective immune system - patients have low levels of lymphocytes (B and T immune cells); this is correlated with severe cases resulting in organ damage - COVID19 patients have vast quantities of antibody-secreting plasmablasts, which seem to persist. There are some studies that suggest that the antibodies produced differ between moderate and severe forms of the disease mostly in the viral proteins they targeted - severe COVID19 patients *lack* a critical antibody creation process (germinal centers in the lymph nodes and spleen); this affects the creation of specialized B and T immune cells. This could be caused by high levels of certain cytokines or because the patients have a defective immune system lacking it altogether - possible inflammatory cascade due to defective B and T immune system production Sources: https://www.the-scientist.com/news-opinion/cells-response-to-sars-cov-2-different-from-flu-rsv-67358 https://science.sciencemag.org/content/369/6504/718 https://www.nature.com/articles/s41591-020-1051-9 https://www.the-scientist.com/news-opinion/immune-biomarkers-tied-to-severe-covid-19-study-67843 https://www.nature.com/articles/s41586-020-2588-y https://www.sciencedirect.com/science/article/pii/S0092867420309934#! https://www.sciencedirect.com/science/article/pii/S0092867420309922 https://science.sciencemag.org/content/369/6508/1210 https://www.nature.com/articles/s41591-020-0901-9 https://immunology.sciencemag.org/content/5/50/eabd6832 https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(20)30118-X https://www.the-scientist.com/news-opinion/differences-in-antibody-responses-linked-to-covid-19-outcomes-67836 https://www.the-scientist.com/news-opinion/some-covid-19-patients-lack-key-structures-for-antibody-creation-67868 https://www.cell.com/cell/fulltext/S0092-8674(20)31067-9 https://www.medrxiv.org/content/10.1101/2020.04.29.20083717v2

Chris
Chris 2 months

Rest in peace sir.

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