Antigenic Complementarity between Influenza A Virus and Haemophilus influenzae may Drive Lethal Co-Infection Such as that Seen in 1918-19 Pandemic

Root‐Bernstein, Robert; Podufaly, Abigail; Aimone, Francesco

doi:10.4172/2324-8955.1000106

Cited by 2 publications

References 38 publications

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Why Infants Rarely Die of COVID-19 and Morbidity and Mortality Rates Vary by Location: Pneumococcal and Hib Vaccinations as Possible Means to Mitigate Future Pandemics

Root‐Bernstein¹

2020

Preprint

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Two conundrums have puzzled COVID-19 investigators: 1) morbidity and mortality is rare among Infants and young children and 2) rates of morbidity and mortality exhibit very large variances across nations, locals and even within cities. These differences correlate with rates of Haemophilus influenzae type B (Hib) and pneumococcal vaccination, which are almost universal among infants and vary widely by geography among adults and the elderly. The higher the rate of vaccination, the lower the COVID-19 morbidity and mortality. Vaccination rates with other vaccines, including BCG and poliovirus, do not correlate with COVID-19 risks. Notably, both Hib and pneumoccoci are common co-infections with influenza and coronaviruses and are associated with more severe disease and risk of death. Whether the vaccines simply protect against COVID-19 complications, directly protect against COVID-19 infection by inducing cross-reactive immunity, or are markers for some other types of protection such as availability of better healthcare, is not yet known. What is known is that improving coverage rates of Hib and pneumococcal vaccination has significantly lowered severe morbidity and mortality in influenza epidemics and might have similar efficacy for mitigating coronavirus outbreaks. If infants and children are valid indicators, the beneficial effects might be very significant. The possibility that anti-viral proteins in milk (e.g., lactoferrin) protect against COVID-19 is also explored.

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Why Infants Rarely Die of COVID-19 and Morbidity and Mortality Rates Vary by Location: Pneumococcal and Hib Vaccinations as Possible Means to Mitigate Future Pandemics

Root‐Bernstein¹

2020

Preprint

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How to Make a Non-Antigenic Protein (Auto) Antigenic: Molecular Complementarity Alters Antigen Processing and Activates Adaptive-Innate Immunity Synergy

Root‐Bernstein¹

2015

ACAMC

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Evidence is reviewed that complementary proteins and peptides form complexes with increased antigenicity and/or autoimmunogenicity. Five case studies are highlighted: 1) diphtheria toxin-antitoxin (antibody), which induces immunity to the normally non-antigenic toxin, and autoimmune neuritis; 2) tryptophan peptide of myelin basic protein and muramyl dipeptide ("adjuvant peptide"), which form a complex that induces experimental allergic encephalomyelitis; 3) an insulin and glucagon complex that is far more antigenic than either component individually; 4) various causes of experimental autoimmune myocarditis such as C protein in combination with its antibody, or coxsackie B virus in combination with the coxsackie and adenovirus receptor; 5) influenza A virus haemagglutinin with the outer membrane protein of the Haemophilus influenzae, which increases antigenicity. Several mechanisms cooperate to alter immunogenicity. Complexation alters antigen processing, protecting the components against proteolysis, altering fragmentation and presenting novel antigens to the immune system. Complementary antigens induce complementary adaptive immune responses (complementary antibodies and/or T cell receptors) that produce circulating immune complexes (CIC). CIC stimulate innate immunity. Concurrently, complementary antigens stimulate multiple Toll-like receptors that synergize to over-produce cytokines, which further stimulate adaptive immunity. Thus innate and adaptive immunity form a positive feedback loop. If components of the complex mimic a host protein, then autoimmunity may result. Enhanced antigenicity for production of improved vaccines and/or therapeutic autoimmunity (e.g., against cancer cells) might be achieved by using information from antibody or TCR recognition sites to complement an antigen; by panning for complements in randomized peptide libraries; or using antisense peptide strategies to design complements.

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Antigenic Complementarity between Influenza A Virus and Haemophilus influenzae may Drive Lethal Co-Infection Such as that Seen in 1918-19 Pandemic

Cited by 2 publications

References 38 publications

Why Infants Rarely Die of COVID-19 and Morbidity and Mortality Rates Vary by Location: Pneumococcal and Hib Vaccinations as Possible Means to Mitigate Future Pandemics

Why Infants Rarely Die of COVID-19 and Morbidity and Mortality Rates Vary by Location: Pneumococcal and Hib Vaccinations as Possible Means to Mitigate Future Pandemics

How to Make a Non-Antigenic Protein (Auto) Antigenic: Molecular Complementarity Alters Antigen Processing and Activates Adaptive-Innate Immunity Synergy

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