Don't wish to Bore you but .........9 May 2020 09:30
is most severe in elderly individuals and resulted in ~52 % mortality among elderly SARS patients [16]. Pathological investigation of patients with lethal SARS revealed acute pulmonary edema, extensive inflammatory cell infiltration, multi-organ failure, thromboembolic complications and septicemia [17]. Severe lung and systemic inflammation is believed to result from cytokine dysregulation; in patients with SARS, increased levels of cytokines such as TNF-a, IP10, IL-6 and IL-8 likely contributed to the poor outcome [17]. Such an exuberant innate cytokine response was attributed to hyper-activation of macrophage/monocyte lineage cells. Additionally, increased levels of type I interferon (IFN) and a dysregulated interferon-stimulated gene (ISG) response were observed in patients with severe SARS [18, 19]. Overall, it is still not known whether SARS in humans was the result primarily of type I IFN-independent exaggerated pro-inflammatory reaction or whether both IFN-dependent and IFN-independent aberrant cytokine production contributed to severe pathology.
""" Severe SARS-CoV infection in humans was characterized by the delayed development of the adaptive immune response and prolonged virus clearance """
Follow-up studies from patients who recovered from SARS suggest that the SARS-CoV-specific antibody response is short lived. In these patients, SARS-CoV-specific IgM and IgA response lasted less than 6 months, while virus-specific IgG titer peaked four-month post-infection and markedly declined after 1 year. Despite the lack of virus-specific memory B cell response, SARS-CoV-specific memory T cells persist in SARS-recovered patients for up to 6 years post-infection. Consistent with these human studies, results from animal studies also suggest that strong virus-specific T cell response are required to protect mice from lethal SARS-CoV-MA15 infection. The future vaccine interventions should also consider strategies to enhance T cell response to provide robust long-term memory. Since, tissue-resident memory T cells provide better protection, boosting a local and systemic memory T cell response would be a useful strategy than either of these interventions alone.
I can only find supporting evidence that if you want a good vaccine ......... you have to have cd4 and Cd8 .... active
so these Parties that cannot elicit a potent T cell response as well as a potent neutralizing antibody response may struggle to prove long term immunity from a vaccine .... indeed it could become useless in less than 6 months ..
Scancell approach is to build a vaccine that achieves at least 6 years immunity with the ability to handle mutations
so what we do know that a neutralizing antibody in the aged population may not be enough .. by the time the adaptive immune system has kicked in ...it may be to late to recover
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