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I was there for Mother Abigail's "debutante ball" on this forum; the ensuing discussion was instrumental for my awareness concerning N-acetylcysteine prophalaxis potentially mitigating cytokine storm. A person that had suffered from lupus told me they'd gone into remission because of it.

My understanding of eschatology suggests that anything approaching to an extinction event will not occur to that conflict that occurs whereby IF BUT FOR the Lord's return: all life on the planet would be extinguished.

Moreover, I'm skeptical about "superinfection" due to neuramindase prophalaxis in that tropism for influenza & HIV are different, albeit that there appears that HIV & either human and avian influenza virion plausibly could share alveoli macrophages as target cells betwixt themselves.

Influenza A virus, together with Influenza B virus, Influenza C virus, Isavirus and Thogotovirus, are the five genera forming the family Orthomyxoviridae. Orthomyxoviridae are enveloped, negative-stranded RNA viruses with a segmented genome. Influenza A viruses can be further categorized into subtypes based on two surface glycoproteins, the hemagglutinin (HA) and the neuraminidase (NA). To date, 16 different HAs and 9 different NAs have been found and may occur in virtually all possible combinations. Free-ranging waterbirds are considered to be the natural reservoir of all influenza A viruses. Even though some mammalian species— humans, pigs, horses and dogs—harbor their own influenza A viruses, there is strong evidence that these mammalian viruses originate from avian influenza A viruses. In addition, avian influenza A viruses may cross the species barrier to other mammals without developing into a stable lineage in the new host species. An example is the outbreak of avian influenza virus of the subtype H7N7 in harbor seals in 1979. Interestingly, the primary replication site for influenza A virus differs between birds and mammals. In birds, the virus replicates primarily in the intestinal tract, whereas in mammals, it replicates primarily in the respiratory tract. An important feature of avian influenza viruses is their capacity to mutate into forms that cause high mortality in poultry. Such mutations only have been recorded for the subtypes H5 and H7 and occur after transmission of these viruses to poultry. Based on their capacity to cause morbidity and mortality in chickens, avian influenza viruses are classified as low pathogenic avian influenza virus (LPAIV) or high pathogenic avian influenza virus (HPAIV). - A Critical Role of Cell Tropism for the Pathogenesis of Influenza (doctroral thesis of Riel, D.A.J. van (published by Erasmus University Rotterdam 2010-09-23)

Human and avian influenza viruses target different cell types in cultures of human airway epithelium (PNAS - Edited by Peter Palese, Mount Sinai School of Medicine, New York, NY, and approved January 30, 2004 (received for review December 3, 2003)

HIV tropism refers to the cell type that the human immunodeficiency virus (HIV) infects and replicates in. HIV tropism of a patient's virus is measured by the Trofile assay.

"T helper - T_h - cells are a sub-group of lymphocytes, a type of white blood cell, that play an important role in the immune system, particularly in the adaptive immune system. These cells have no cytotoxic or phagocytic activity; they cannot kill infected host cells or pathogens. Rather, they help other immune cells—they activate and direct other immune cells. They are essential in B cell antibody class switching, in the activation and growth of cytotoxic T cells, and in maximizing bactericidal activity of phagocytes such as macrophages.

Mature Th cells express the surface protein CD4 and are referred to as CD4+ T cells. CD4+ T cells are generally treated as having a pre-defined role as helper T cells within the immune system. For example, when an antigen presenting cell expresses an antigen on MHC class II, a CD4+ cell will aid those cells through a combination of cell to cell interactions (e.g. CD40 and CD40L) and through cytokines." - T helper cell (from the Wiki)

The foregoing notwithstanding, I'm greatly appreciative of MA's superior knowlege concerning virion science; I'm certain she's forgotten more than I'll ever know about the matter. Although her arguments are compelling, I'm unconvinced that what she fears will actually manifest itself to the degree she alludes to.

"My understanding of eschatology suggests that anything approaching to an extinction event will not occur to that conflict that occurs whereby IF BUT FOR the Lord's return: all life on the planet would be extinguished."

S/r:

My understanding of eschatology suggests that anything approaching to an extinction event will not occur prior to that conflict that occurs whereby IF BUT FOR the Lord's return: all life on the planet would be extinguished.

These cells have no cytotoxic or phagocytic activity; they cannot kill infected host cells or pathogens. Rather, they help other immune cells—they activate and direct other immune cells.

That is how I interpreted it. What if they become aerosolized?

You sound like MA. Meaning, I have to go Huh?

Great post. I will try to pretend to understand give a reasonable answer.

There is a bit of confusion about the flu and HIV (I hope it is not in my writing).

There is no part of her thesis that hypothesizes that influenza and HIV will join or swap genes.

Her concern is that under no circumstances should we be messing with the nerumindase in a HIV infected patient.

Boosting, inhibiting - nothing!

She explains that neuraminidase is a known mutanagenic enhancer for HIV and it is stupid to be messing with it in a patient who is HIV positive.

HIV is already a mutant producing machine, making zillions of variations daily trying to break out.

And to purposefully administer any drug that disrupts neuraminidase regulation in a HIV carrier is suicide.