#HerpesVirus
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stacyhorn.bsky.social
I’m always posting about other people’s pets, but I have 3 cats myself (& long to add a dog to the mix). This is Bleecker, at the vet, AGAIN. He has been diagnosed with diabetes, feline herpesvirus, & IBD. He’s just started having nose bleeds. And I am $700+ poorer.
January 30, 2026 at 3:50 PM
Role of γδ T cells in turkey herpesvirus vaccine protection against Marek’s disease virus

www.microbiologyresearch.org/content/jour...
www.microbiologyresearch.org
January 30, 2026 at 3:29 PM
themestimes.bsky.social
A mother in the United Kingdom said doctors first thought her 16-month-old son, Juwon, had a simple eye infection when his symptoms began in August 2024.

#HealthNews #UKNews #ChildHealth #MedicalAwareness #EyeHealth #HerpesVirus
January 30, 2026 at 3:29 PM
instruct-eric.bsky.social
Integrated structural biology at its best with fantastic talks in cryo-EM, NMR, and X-ray techniques
Also integration with other Instruct Centres, in this case Kay Grünewald Instruct-DE @cssbhamburg.bsky.social 'Conformational flexibility and molecular plasticity in herpesvirus entry and egress'
January 29, 2026 at 4:48 PM
statto.bsky.social
Herpesvirus number…

1 & 2. HSV-1 & 2, genital herpes/cold sores. Chronic infections—cold sores keep coming back once you’ve been infected.

3. Chickenpox, later shingles. Linked to dementia in later life—there’s growing evidence that the shingles vaccine is protective.

4. EBV (see above).
January 29, 2026 at 9:36 AM
isanthropia.bsky.social
Shingles is the re-activated VCV - a herpesvirus. You get chicken pox then the virus lies dormant on nerve endings. Once reactivated, it actually gooses our stress hormones even higher so it can replicate faster. Perhaps all herpesviruses have a role in the development of dementia in later life. 2/
January 28, 2026 at 5:50 PM
mclellanlab.bsky.social
Our third installment on prefusion stabilization of herpesvirus gB proteins is available as a preprint: doi.org/10.64898/202.... A great collaboration with colleagues at Merck. Our prefusion HSV-2 gB protein adopts a more closed conformation than has been observed for HSV-1 gB in recent papers.
January 27, 2026 at 8:53 PM
johnbirchman.bsky.social
What if you are talking about Robert Hegyes from Welcome Back Kotter?
Or the human herpesvirus 4 (HHV-4) virus, EBV?
Or the thousands of scientists, mathematicians, musicians, artists, athletes, and numerous other people that share that name? 🤔
January 27, 2026 at 4:36 AM
tomkindlon.bsky.social
ME Research UK:

We recently reported on research suggesting endothelial senescence (aging of the endothelium cells) may lead to endothelial dysfunction in ME/CFS & long COVID.

We have a collection of articles on endothelial dysfunction in #MECFS. Read more: tinyurl.com/endodysme

#cfs #LongCovid
Endothelial dysfunction in ME/CFS The endothelium - a thin layer of cells lining every blood vessel - plays a pivotal role in regulating blood flow, blood clotting, and inflammatory responses. Research suggests that ME/CFS may involve damage to the endothelium leading to endothelial dysfunction (improper functioning of the endothelium). ME/CFS research suggests: significantly impaired endothelial function in both small and large vessels compared to healthy controls endothelial senescence (aging) leading to endothelial dysfunction herpesvirus infection, such as Epstein-Barr virus (EBV) and HHV-6, could contribute to damage of endothelium • • "--1-■111P- I-endothelial cells lining blood vessel • _.■116._ reduced nitric oxide production in ME/CFS may suggest mechanism of endothelial dysfunction - increased microRNAS in ME/CFS indicate endothelial dysfunction endothelial dysfunction may contribute to orthostatic intolerance in ME/CFS INFORM. INFLUENCE. INVEST. UK'
January 26, 2026 at 5:35 PM
longcovidfam.bsky.social
The authors argue that longer treatment with multiple antiviral drugs targeting viral persistence and herpesvirus reactivation might help some Long COVID patients. They say these results support running a larger randomized, double-blind, placebo-controlled trial of IMC-2 + Paxlovid.​​​​​​​​​​​​​​​​
January 23, 2026 at 1:20 PM
cryoempapers.bsky.social
Conserved assembly architecture of the essential herpesvirus packaging accessory factor www.biorxiv.org/content/10.64898/2026.01.22.701024v1 #cryoem
January 23, 2026 at 10:05 AM
biorxivpreprint.bsky.social
Conserved assembly architecture of the essential herpesvirus packaging accessory factor https://www.biorxiv.org/content/10.64898/2026.01.22.701024v1
January 22, 2026 at 11:17 PM
biorxiv-microbiol.bsky.social
Conserved assembly architecture of the essential herpesvirus packaging accessory factor https://www.biorxiv.org/content/10.64898/2026.01.22.701024v1
January 22, 2026 at 11:17 PM
readtrajectory.bsky.social
Varicella-zoster reactivation causes serious inflammation in older adults, so dampening that cascade could plausibly affect aging markers. Would be interesting to see if other live-attenuated vaccines show similar patterns, or if it's specific to herpesvirus suppression.
January 22, 2026 at 4:17 PM
zezenzuska.bsky.social
Miau qué, MIAU QUÉ - Ambos

Sin morder... SIN MORDER, COPÓN - Fleck, cariñoso conmigo

Deja en paz a tu hermana - Fleck, dando por culo a Clio

A ver esas legañas - Clio, con herpesvirus

Pero qué bruta eres - Clio, destrozando cualquier juguete
January 22, 2026 at 11:57 AM
Nucleus softens during herpesvirus infection

journals.plos.org/plospathogen...
Nucleus softens during herpesvirus infection
Author summary DNA viruses take over the host cell nucleus, inducing dramatic structural modifications. There is currently very little knowledge of how the progression of viral infection modifies the ...
journals.plos.org
January 21, 2026 at 1:41 PM
biorxiv-microbiol.bsky.social
Bacteria-herpesvirus interaction reveals a proviral role of ISGylation in promoting herpesvirus capsid assembly https://www.biorxiv.org/content/10.64898/2026.01.19.700396v1
January 21, 2026 at 2:17 AM
biorxivpreprint.bsky.social
Bacteria-herpesvirus interaction reveals a proviral role of ISGylation in promoting herpesvirus capsid assembly https://www.biorxiv.org/content/10.64898/2026.01.19.700396v1
January 21, 2026 at 2:17 AM
johngosland.bsky.social
Feline herpesvirus? Beautiful boy but my dear cat Wubz gets similar wet eyes and raw nose. Common for cats that come from the shelter.

Sending love to all and sorry for the loss 🖤🖤🖤
January 20, 2026 at 3:18 AM
kratzdiebuerste.bsky.social
Kann bitte irgendjemand das Scheiß Herpesvirus ausrotten?
Ich. Bin. Genervt.
January 18, 2026 at 6:49 PM
castltrastondrs.bsky.social
may drive chronic inflammation & facilitate the reactivation of latent pathogens such as EBV & human herpesvirus 6 (HHV-6).
- Clinical Vulnerability - Sustained subnormal immune cell counts may reduce the "margin of safety" against new infections & impair surveillance against emerging cancers
January 17, 2026 at 3:29 PM
charitychicken.bsky.social
1/2 “In summary, our longitudinal reveals persistent humoral, cellular, and molecular immune dysregulation in individuals with LC. We demonstrate that IgG antibodies in LC participants exhibit persistent skewing in SARS-CoV-2 antigen recognition, …”
page 15 Discussion Here, we studied the humoral, cellular and molecular indicators of a potential immune dysregulation over time in participants suffering from LC and those who did not exhibit any persistent symptoms after a resolved SARS-CoV-2 infection. Our study shows a distinct shift in the SARS-CoV-2-specific antibody profile with dominant IgG responses to Envelope and Nucleocapsid viral proteins in individuals with LC over the period of at least 6 months after the initial infection. Further analysis determined a close correlation of high Envelope-specific IgG titers with elevated proportions of circulating MAIT cells as well as an increase in the cTFH during LC. Additionally, LC participants exhibited an inflammatory cytokine signature and developed distinct autoreactive antibody responses. Among the many hypotheses regarding the underlying mechanisms of LC, a dysregulation of the immune system has emerged as a prominent pathogenic mechanism. In our study the elevated anti-Envelope and anti-Nucleocapsid IgG response in LC suggest an ongoing antigenic stimulation and suggests persistence of viral proteins or protein fragments in chronically ill individuals. Although all participants in both study cohorts reported a positive vaccination status (Table 1), the higher anti-Spike IgG titers observed in the CONV cohort may suggest a more efficient vaccine-induced response in this group. This interpretation is further supported by our data of predominant Spike-specific IgG4 levels in CONV participants (Fig. 1d), consistent with previous reports demonstrating high IgG4 class-switching of Spike-specific IgG response in individuals who received multiple doses of a mRNA vaccine. IgG4 inherently has an altered capacity to efficiently bind Fc receptors leading to reduced antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) related events. CONTINUES IN NEXT IMAGE… Cont. from prior image: In contrast, IgG3 can effectively bind IgG-Fc-receptor and induce NK cell mediated ADCC. Therefore, it is plausible that LC patients experience more inflammation-prone events due to the persistence of elevated IgG3, while the control group having higher levels of the less inflammatory IgG4 is comparatively protected. This image/pg 16: The overall IgG titer against Spike, albeit lower in the LC group, remained stable over time for up to 6 months after acute infection in contrast to the convalescent group where Spike-specific IgG response diminished at later timepoints. Such a pattern may suggest a sustained immunogenic stimulus in LC, potentially driven by persistent presence of viral antigens or delayed resolution of immune activation. The exact reason of high immunogenicity of Envelope and Nucleocapsid proteins (but not Spike or Membrane) in LC remains unclear, but the consistency of IgG responses within our cohort supports the hypothesis of a prolonged Envelope and Nucleocapsid viral antigen exposure. The precise location of the latent residual SARS-CoV-2 virus or viral RNA and the tissue serving as a reservoir for ongoing antigenic shedding cannot be ascertained from the analysis of circulating peripheral blood. Our mass spectrometry analysis of plasma proteome revealed elevated IgA and IgM immunoglobulin and J-chain peptides in LC participants, along with elevated levels of Ig variable region peptides but none of the IgG subclasses (Fig. 2). This supports the notion of de novo immune activation, especially at mucosal sites, and may suggest that intestinal and lung mucosa may serve as a location for viral persistence and sustained immune stimulation. Reactivation of other latent viruses such as Epstein-Barr virus (EBV) during or following SARS-CoV-2 infection has been increasingly recognized as a putative contributor to the immunopathogenesis of LC. CONTINUES IN NEXT IMAGE… Cont. from prior: Though our analysis focused on SARS-CoV-2-specific immune response, our proteomic analysis showing elevated plasma levels of IGHA, IGHM, and immunoglobulin variable region peptides may reflect mucosal antibody activity which is consistent with EBV’s tropism for the oropharyngeal and gastrointestinal epithelium. Lytic EBV replication in epithelial cells induces the expression of pro-inflammatory mediators, including IL-6 family cytokines such as LIF and IL-11 (Fig. 5), as well as BAFF, which may collectively promote local B cell activation and polyclonal expansion of mucosal antibody-secreting cells. These findings are consistent with the possibility that EBV or other herpesvirus reactivation, together with ongoing SARS-CoV-2 antigenic exposure, may contribute to the systemic immune alterations observed in LC. This page 17: Our immunophenotyping of PBMCs revealed significant alterations in individuals with LC compared to convalescent controls, specifically in the frequencies of circulating TFH, CD4+ TCM and MAIT cells. Elevated proportions of circulating TFH likely indicate their critical role in B cell activation, and the generation of high-affinity antibodies during the acute but also post-acute phases of the infection. The surge of cTFH and CD4+ TCM cells also suggests a persistent ongoing T-cell driven immune response and dysregulated B cell activity. One possibility is that persistent antigen exposure, potentially due to viral protein reservoir or latent viral reactivation, sustains TFH cell differentiation and circulation. Alternatively, this could indicate altered trafficking or retention of TFH-like cells outside of secondary lymphoid tissues. Elevated frequencies of cTFH could contribute to prolonged or atypical antibody responses, including those observed in our proteomic analyses showing sustained Envelope- and Nucleocapsid-specific IgG titers in LC, as well as elevated mucosal immunoglobulin signature in the plasma proteome. CONTINUES… Cont.: Elevated presence of MAIT cells in peripheral blood during LC is indicative of systemic immune activation, altered tissue trafficking, or an ongoing mucosal immune stimulation. During acute SARS-CoV-2 infection, MAIT cells undergo significant perturbation, exhibiting activation during acute disease followed by numerical alterations and functional impairments. Interestingly, in our study, LC participants demonstrate sustained elevation of MAIT cell frequencies for at least 6 months post-acute infection. This persistence strongly correlates with heightened IgG titers against the SARS-CoV-2 Envelope protein, suggesting a prolonged immune activation state that is absent in convalescent individuals. In fact, in an animal model of SARS-CoV-2 infection, MAIT cells have been shown to provide help to B cells and enhance Ab response. This raises important questions regarding MAIT cell involvement in the pathogenesis of LC. Their continued presence could indicate chronic inflammatory signaling, potentially mediated by IL-18 and IL-12 or other combination of inflammatory cytokines, leading to dysregulated immune responses. Moreover, the sustained anti-Envelope IgG levels point to ongoing B cell activity, which may be influenced by MAIT cell-derived cytokines such as IFN-γ and IL-17. In chronic viral infections like HIV and hepatitis, MAIT cells frequently exhibit exhaustion phenotypes, contributing to disease persistence rather than This page 18: resolution. A similar mechanism may be at play in LC, where sustained MAIT activation perpetuates inflammatory cascades, leading to lingering symptoms. The interplay between prolonged MAIT activity and persistent B cell activation necessitates further exploration, as it could provide valuable insights into the immune dysregulation characteristic of LC. CONTINUES IN NEXT IMAGE IN NEXT REPLY TO THIS POST.
January 17, 2026 at 2:34 PM
merz.bsky.social
EBV is a herpesvirus. Unlike SARS-CoV-2 or RSV, we don't clear the infection — we only suppress it. The viral genomes integrate into our genomes, and they're with us for life.
January 15, 2026 at 4:16 PM
npfmorsan.mastodonsweden.se.ap.brid.gy
Lite hoppfullt om möjlig medicin och vaccin mot MS i framtiden. Kopplat till T celler. Forskning visar hur virus lurat kroppen att börja angripa sig själv för vissa personer.

https://www.dn.se/sverige/sa-kan-ett-vanligt-herpesvirus-leda-till-ms/
Så kan ett vanligt herpesvirus leda till ms
Viruset Epstein-Barr har länge kopplats till multipel skleros (ms). Nu har svenska forskare hittat en förklaring till hur viruset skadar hjärnan.
www.dn.se
January 13, 2026 at 8:17 PM
dgspsoa.bsky.social
nötige Energie zum Reifen besitzen. Da diese Zellen hauptsächlich für die Beseitigung von Krankheitserregern verantwortlich sind, könnte ihr relativer Mangel erklären, warum Menschen mit ME/CFS Schwierigkeiten haben, Infektionen oder Herpesvirus-Reaktivierungen abzuwehren.

4/10 ⬇️
January 13, 2026 at 7:46 PM