I am not sure if I lost the sound, but here is a ppt presentation posted last September 9, on how SARS-CoV-2 targets the critical HERV-K102 innate immunity protection system including the induction of immunosenescence. Immunosenescence is the key risk factor for COVID-19 severity (causes chronic diseases associated with aging, stress and involves infections). In 2015 I defined immunosenescence (at the level of macrophages) as the failed lytic release of HERV-K102 protector particles from foamy macrophages [Laderoute M, Discovery Medicine, 2015].
A week or so after posting, a new paper indirectly substantiated that HERV-K102 activation protects against severity. At the time of acute COVID-19 hospital admission an analysis of circulating monocytes revealed that those patients with upregulated IRF1 and an M1 profile were less likely to be admitted to ICU or were at significantly reduced risk of death [Utrero-Rico A et al., Biomedicines, September 17, 2021]. In other words this phenotype consistent with HERV-K102 early activation was found to protect against COVID-19 severity.
In terms of the first two slides, it should be noted that one dose of mRNA vaccine is associated with the induction of trained immunity (putative HERV-K102 induction) whereas two doses induces adaptive immunity antibodies (including neutralizing and enhancing). One mRNA dose via trained immunity provides heterologous protection reducing non-COVID all cause mortality by about 60 to 70 % [Xu S et al, MMWR 2021] whereas the second dose does not appreciably change anything. It is only when the person then becomes infected with SARS-CoV-2 that ADE mediates infection into foamy macrophages via BSG and cancels the heterologous protection (of trained innate immunity).
How SARS-CoV-2 Targets Trained Immunity Involving HERV-K102 Particle Production