{"id":3034,"date":"2023-03-28T19:19:16","date_gmt":"2023-03-29T00:19:16","guid":{"rendered":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/?p=3034"},"modified":"2023-03-28T19:22:04","modified_gmt":"2023-03-29T00:22:04","slug":"mrna-vaccine-beats-infection-for-key-defense-against-covid-19-stanford-medicine-scientists-find","status":"publish","type":"post","link":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/2023\/03\/28\/mrna-vaccine-beats-infection-for-key-defense-against-covid-19-stanford-medicine-scientists-find\/","title":{"rendered":"mRNA vaccine beats infection for key defense against COVID-19, Stanford Medicine scientists find"},"content":{"rendered":"
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(Stanford Medicine<\/a>) Stanford Medicine researchers have shown that prior SARS-CoV-2 infection reduces killer T cells\u2019 response to vaccination. These cells are crucial for eliminating the virus from the body. <\/p>\n\n\n\n

The Pfizer\/BioNTech mRNA vaccine directed at COVID-19 is much better than natural infection at revving up key immune cells called killer T cells to fight future infection by SARS-CoV-2, the virus that causes COVID-19, Stanford Medicine investigators have found.<\/p>\n\n\n\n

The scientists also showed, in a study<\/a> published online in Immunity<\/em>, that getting infected by SARS-CoV-2 before getting vaccinated lowers the vaccine\u2019s otherwise exceptional ability to spur proliferation and activation of killer T cells directed at SARS-CoV-2. Their finding suggests that those hoping to avoid the manifold health risks associated with COVID-19 would do well to get vaccinated before they contract the disease.<\/p>\n\n\n\n

The good news is that vaccination after having had COVID-19 does somewhat boost the numbers and battle-readiness of this SARS-CoV-2-infection-impaired killer T cell population \u2014 just not nearly as much as if vaccination had preceded infection.<\/p>\n\n\n\n

Although the study didn\u2019t directly demonstrate it, killer T cells\u2019 lost punch after a bout of COVID-19 could spell a weakened immune response to a new SARS-CoV-2 assault later, boosting the odds that the virus will persist in overlooked infected cells and possibly contributing to the development of long COVID, suggested Mark Davis<\/a>, PhD, professor of microbiology and immunology and a Howard Hughes Medical Institute investigator.<\/p>\n\n\n\n

Davis, who is also the Burt and Marion Avery Family Professor, is the study\u2019s senior author. Sharing lead authorship are postdoctoral scholars Vamsee Mallajosyula, PhD, and Fei Gao, PhD.<\/p>\n\n\n\n

In contrast with antibodies, which are immune-generated proteins that can prevent a virus from getting inside our cells and kicking off infections, <\/a><\/a>killer T cells roam through our bodies\u2019 tissues, inspect cells\u2019 surfaces for telltale traces of infectious pathogens and kill infected cells.<\/p>\n\n\n\n

A given killer T cell responds to only one of those telltale traces, or at most to a handful of them. In principle, it will attack only one type of pathogen.<\/p>\n\n\n\n

While the body\u2019s gigantic repertoire of killer T cells typically contains numerous cells recognizing various features of that pathogen, the vast majority of cells in that massive repertoire remain at ease. For that reason, an infection by one particular virus won\u2019t generate an exhaustive \u2014 and exhausting \u2014 immune response to every microbial invader under the sun.<\/p>\n\n\n\n

If, for any reason, killer T cells aren\u2019t abundant enough or don\u2019t get sufficiently activated, a virus that has ducked the body\u2019s antibody defense and established a beachhead inside a cell gets extra time to commandeer that cell\u2019s productive machinery, forcing it to produce copious copies of the virus and send its progeny off to invade other cells.<\/p>\n\n\n\n

Investigating the vaccine<\/h3>\n\n\n\n

Soon after the Pfizer-BioNTech-designed COVID-19 vaccine became available, Davis, who directs Stanford\u2019s\u00a0Institute for Immunity, Transplantation and Infection<\/a>, and his colleagues set out to determine how it worked. (No equivalent analysis was performed on the Moderna vaccine.) <\/p>\n\n\n\n

Most investigations of vaccine efficacy have focused on these products\u2019 ability to generate antibodies, whose infection-blocking effectiveness can be measured in laboratory glassware with relative ease. T cells have proved tougher to study. But Davis, who over several decades has pioneered the exploration of killer T cells and their cousins, helper T cells, has advanced their analysis by designing and championing ever-better methods for monitoring their more complex and more subtle interactions with their targets.<\/p>\n\n\n\n

Helper T cells, more managerial in nature than killer T cells, are instrumental in inducing antibody production by another immune-cell type called B cells.<\/p>\n\n\n\n

Davis noted that the way T cells recognize antigens differs from the way antibodies recognize antigens, rendering T cells less likely to be fooled and defeated by tiny mutations in viral sequence (strain variants) than antibodies.<\/p>\n\n\n\n

For the new study, Davis and his colleagues were armed with state-of-the-art technology, pioneered by Mallajosyula in Davis\u2019 lab, that permitted them to precisely measure changes in levels of killer T cells directed specifically at cells infected by SARS-CoV-2. The researchers analyzed blood samples from three categories of study participants: people with no history of prior SARS-CoV-2 infection who were getting their first and second doses of the new mRNA vaccine, unvaccinated COVID-19 patients, and those getting the vaccine who\u2019d previously been infected by the virus but who had now recovered \u2014 at least, apparently.<\/p>\n\n\n\n

The researchers monitored the proliferation and activation of killer T cells specifically directed against SARS-CoV-2 in these individuals, drawing blood at several time points starting on the day of their first vaccine dose \u2014 or, in unvaccinated COVID-19 patients, on the first day they manifested symptoms.<\/p>\n\n\n\n

Uninfected vaccine recipients experienced a greater than 60-fold rise in their levels of SARS-CoV-2-targeting killer T cells. By six weeks after their first dose, one in every five of their killer T cells was SARS-CoV-2-specific.<\/p>\n\n\n\n

COVID-19 patients showed more lackluster results: Average levels of their total SARS-CoV-2-specific killer T cells were less than one-tenth those of infection-free vaccinees \u2014 despite the fact that the vaccine contains only one part of the virus (the so-called spike protein SARS-CoV-2 uses to latch onto cells) while infection by the actual virus can generate killer T cell responses to multiple components.<\/p>\n\n\n\n

Recovered COVID-19 patients\u2019 SARS-CoV-2-specific response to vaccination also lagged behind that of never-infected participants\u2019 response. Three weeks after the second dose of the two-dose mRNA-vaccine regimen, killer T cells narrowly targeting SARS-CoV-2 were less than one-seventh as prevalent in previously infected vaccinees\u2019 blood as they were in the blood of never-infected vaccinees at the same time point. These cells, moreover, seemed less warlike, by virtue of the signaling substances they secreted, in previously infected than in never-infected vaccine recipients.<\/p>\n\n\n\n

Helper T cells were not strongly affected by prior SARS-CoV-2 infection. In contrast to killer T cells\u2019 in-your-face behavior, these cells play a more managerial role. This includes encouraging antibody production by other immune cells called B cells.<\/p>\n\n\n\n

Antibody production upon reinfection of former SARS-CoV-2 patients remains robust, Davis said.<\/p>\n\n\n\n

\u201cBut antibodies mostly only block infection \u2014 they\u2019re much less able to root out established infections,\u201d he said. \u201cOnly killer T cells can do that. We think the infection-induced shortage of functional killer T cells may be one factor that\u2019s helping give rise to long COVID, because these impaired killer T cell populations aren\u2019t adequately eliminating all infected cells \u2014 and they\u2019re becoming exhausted in trying to do so.\u201d<\/p>\n<\/div><\/div>","protected":false},"excerpt":{"rendered":"

(Stanford Medicine) Stanford Medicine researchers have shown that prior SARS-CoV-2 infection reduces killer T cells\u2019 response to vaccination. These cells are crucial for eliminating the virus from the body. The Pfizer\/BioNTech mRNA vaccine directed at COVID-19 is much better than natural infection at revving up key immune cells called killer T cells to fight future […]<\/p>\n","protected":false},"author":11,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_jetpack_memberships_contains_paid_content":false,"footnotes":"","jetpack_publicize_message":"mRNA #Vaccine v #COVID infection guess the winner for better protection @StanfordMed @pfizer #killertcells \n\ud83d\udcaa ","jetpack_publicize_feature_enabled":true,"jetpack_social_post_already_shared":false,"jetpack_social_options":{"image_generator_settings":{"template":"highway","default_image_id":0,"font":"","enabled":false},"version":2}},"categories":[8],"tags":[],"class_list":["post-3034","post","type-post","status-publish","format-standard","hentry","category-vaccine-headlines"],"jetpack_publicize_connections":[],"jetpack_featured_media_url":"","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/posts\/3034","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/users\/11"}],"replies":[{"embeddable":true,"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/comments?post=3034"}],"version-history":[{"count":1,"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/posts\/3034\/revisions"}],"predecessor-version":[{"id":3035,"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/posts\/3034\/revisions\/3035"}],"wp:attachment":[{"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/media?parent=3034"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/categories?post=3034"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.unmc.edu\/healthsecurity\/transmission\/wp-json\/wp\/v2\/tags?post=3034"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}