#Herpesvirus
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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
mazapanes.bsky.social
Conjuntivitis (casi seguro que es un herpesvirus) 😔
January 13, 2026 at 7:21 PM
reactome.org
The Journal of #Virology article "Inhibition of type I interferon signaling is a conserved function of gamma-herpesvirus-encoded microRNAs", examines how gamma-herpesviruses from non-human primates use microRNAs to suppress type I interferon signaling.
January 13, 2026 at 3:48 PM
microbiologysociety.org
A new study provides a detailed overview of the deadly Ostreid herpesvirus 1 (OsHV-1) lifecycle in Pacific oysters. Their findings also reveal how host genetics can influence the immune response and infection outcomes to OsHV-1.

Read the article here🔗 doi.org/10.1099/jgv....
January 12, 2026 at 1:00 PM
mecfs-pinguin.bsky.social
Menschen mit ME/CFS ▫️Schwierigkeiten haben, Infektionen oder Herpesvirus- Reaktivierungen abzuwehren❗

📍Diese reifen Immunzellen sind auch für die Beseitigung von
▫️Gewebeschäden,
▫️Darmpermeabilität, ▫️Blutgefäßproblemen usw. verantwortlich, die typischerweise vorübergehend durch Anstrengung
January 11, 2026 at 8:14 PM
diarioveterinario.com
La identificación del herpesvirus se llevó a cabo mediante técnicas moleculares realizadas en muestras obtenidas de esas lesiones vesiculares
Veterinarios españoles participan en el descubrimiento de un nuevo virus en perezosos
Un equipo internacional integrado por investigadores y veterinarios de la Universidade de São Paulo y el Aquário de São Paulo –ambos de Brasil– y del centro español CISA-INIA/CSIC ha descubi ...
mlibr.es
January 11, 2026 at 9:02 AM
pt-noticias.bsky.social
Vírus da herpes já infectavam humanos há mais de 2.000 anos, revela DNA antigo

https://www.europesays.com/pt/223233/

Cientistas de diversas universidades europeias identificaram, pela primeira vez, genomas antigos de herpesvírus humanos preservados no DNA de…
Vírus da herpes já infectavam humanos há mais de 2.000 anos, revela DNA antigo - Portugal
Cientistas de diversas universidades europeias identificaram, pela primeira vez, genomas antigos de herpesvírus humanos preservados no DNA de esqueletos com
www.europesays.com
January 10, 2026 at 8:00 AM
cryoempapers.bsky.social
Monoclonal neutralizing antibodies elicited by infection with Kaposi sarcoma-associated herpesvirus reveal critical sites of vulnerability on gH/gL pubmed.ncbi.nlm.nih.gov/41499715/ #cryoem
January 9, 2026 at 5:15 AM
diarioveterinario.com
Un equipo internacional integrado por investigadores y veterinarios de la Universidade de São Paulo y el Aquário de São Paulo –ambos de Brasil– y del centro español CISA-INIA/CSIC ha descubierto un nuevo herpesvirus en perezosos
Veterinarios españoles participan en el descubrimiento de un nuevo virus en perezosos
Un equipo internacional integrado por investigadores y veterinarios de la Universidade de São Paulo y el Aquário de São Paulo –ambos de Brasil– y del centro español CISA-INIA/CSIC ha descubi ...
mlibr.es
January 8, 2026 at 3:04 PM
lancasterfarming.bsky.social
The recent equine herpesvirus myeloencephalopathy has given horse owners renewed reason to keep these biosecurity measures in mind in the barn and while they travel.
Infectious Disease Biosecurity for Horse Farms and Owners
The recent equine herpesvirus myeloencephalopathy has given horse owners renewed reason to keep these biosecurity measures in mind in the barn and while they travel.
www.lancasterfarming.com
January 7, 2026 at 1:52 PM
enirenberg.bsky.social
We don't actually know what happens to cause shingles outbreaks in detail, but we see it in immunologically competent people, too. Stress has been proposed as a cause, and the evidence there is mixed. Fever is a known trigger of herpesvirus reactivation. Unfortunately, we just don't know.
January 6, 2026 at 6:46 PM
valebodi.bsky.social
Does Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Represent a Poly-Herpesvirus Post-Virus Infectious Disease?
by Maria Eugenia Ariza, Irene Mena Palomo and Marshall V. Williams
(December 2025)

#ME/CFS #HHVs #dUTPase
www.mdpi.com
January 6, 2026 at 5:39 PM
lucibee.bsky.social
...and 15 years ago, Martin Lerner was developing treatment protocols on this basis in the US.

"We propose that ME/CFS patients have nonpermissive
herpesvirus (EBV, HCMV, HHV6) replication, expressing
immediate-early (IE) gene products, which induce host
cell dysregulation and host cell apoptosis."
www.dovepress.com
January 6, 2026 at 12:05 PM
mecfsskeptic.bsky.social
5) Link to the hypothesis paper:

Ariza et al. 2025. Does Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Represent a Poly-Herpesvirus Post-Virus Infectious Disease?
pubmed.ncbi.nlm.nih....
January 6, 2026 at 9:34 AM
es-noticias.bsky.social
Un estudio revela que los herpesvirus llevan miles de años formando parte del genoma humano

https://www.europesays.com/es/325622/

Un grupo de científicos de la Universidad de Viena (Austria) y la Universidad de Tartu (Estonia) ha reconstruido…
Un estudio revela que los herpesvirus llevan miles de años formando parte del genoma humano - España
Un grupo de científicos de la Universidad de Viena (Austria) y la Universidad de Tartu (Estonia) ha reconstruido por primera vez genomas antiguos del
www.europesays.com
January 6, 2026 at 8:00 AM