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Samuel Osanyinlusi (He/Him)

@medicsam.bsky.social
7 followers 10 following 2 posts

| Dr.rer.nat. | Herpes Virologist | HCMV | Viral latency & reactivation | DAAD Scholar | Lover of God🇳🇬🇩🇪🇺🇸

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Reposted by Samuel Osanyinlusi (He/Him)
virologyunmasked.bsky.social @virologyunmasked.bsky.social · 16/11/2025
Our first visiting trainee blog! Samuel Osanyinlusi @medicsam.bsky.social has published his first article on our site: "New territory comes with new cultures – how my experiences in Europe compare with America." Check it out! virologyunmasked.com/new-page/
virologyunmasked.com
New territory comes with new cultures
New territory comes with new cultures – how my experiences in Europe compare with America by Dr. Samuel Osanyinlusi – November 15th, 2025 Photo of Dr. Samuel Osanyinlusi Over the last e…
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Reposted by Samuel Osanyinlusi (He/Him)
Samuel Osanyinlusi (He/Him) @medicsam.bsky.social · 23/09/2025
Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation | Journal of Virology journals.asm.org/doi/full/10....
journals.asm.org
Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation | Journal of Virology
Cytomegalovirus (CMV) is a ubiquitous human herpesvirus, infecting the majority of the population worldwide. As with all herpesviruses, once an individual is infected with CMV, the virus remains in the person’s blood cells for life in a silenced state called latency, and this infection, for the most part, remains asymptomatic. When an infected individual’s immune system fails to function properly, however, CMV can become active (termed viral reactivation), which allows the virus to replicate and cause downstream disease. Our understanding of the cellular and viral factors that dictate this switch from silenced to activated remains incomplete. Here, we show a viral protein, UL78, is required for this switch. We find that UL78 helps to reshape cellular signaling, changing the cell environment from one that favors latency to one that supports reactivation. This highlights a new avenue for therapeutic intervention to prevent CMV reactivation and downstream disease.
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Samuel Osanyinlusi (He/Him) @medicsam.bsky.social · 23/09/2025
Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation | Journal of Virology journals.asm.org/doi/full/10....
journals.asm.org
Human cytomegalovirus-encoded G protein-coupled receptor (GPCR) UL78 regulates viral reactivation | Journal of Virology
Cytomegalovirus (CMV) is a ubiquitous human herpesvirus, infecting the majority of the population worldwide. As with all herpesviruses, once an individual is infected with CMV, the virus remains in the person’s blood cells for life in a silenced state called latency, and this infection, for the most part, remains asymptomatic. When an infected individual’s immune system fails to function properly, however, CMV can become active (termed viral reactivation), which allows the virus to replicate and cause downstream disease. Our understanding of the cellular and viral factors that dictate this switch from silenced to activated remains incomplete. Here, we show a viral protein, UL78, is required for this switch. We find that UL78 helps to reshape cellular signaling, changing the cell environment from one that favors latency to one that supports reactivation. This highlights a new avenue for therapeutic intervention to prevent CMV reactivation and downstream disease.
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Samuel Osanyinlusi (He/Him) @medicsam.bsky.social · 17/07/2025
Paper Accepted🎉 details soon..,
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