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Viruses
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Post-Viral Syndromes Following Respiratory Virus Infections: Virological Mechanisms, Therapeutic Approaches,...
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Post-Viral Syndromes Following Respiratory Virus Infections: Virological Mechanisms, Therapeutic Approaches, and Long-Term Management

A Special Issue of Viruses (ISSN 1999-4915) belonging to the section "Coronaviruses".

Deadline for manuscript submissions: closed (7 June 2026) | Viewed by 1985

Editors

Prof. Dr. Oleksandr Kamyshnyi

E-Mail Website
Guest Editor
Department of Microbiology, Virology, and Immunology, I. Horbachevsky Ternopil National Medical University, 46001 Ternopil, Ukraine
Interests: microbiota; immune system; transcriptiome; experimental pathology; metagenomics; intestinal microbiome; diabetes; COVID-19
Special Issues, Collections and Topics in MDPI journals
Dr. Pavlo Petakh

E-Mail Website
Guest Editor
Department of Biochemistry and Pharmacology, Uzhhorod National University, Uzhhorod, Ukraine
Interests: Leptospirosis; COVID-19; diabetes; stress
Dr. Iryna Halabitska

E-Mail Website
Guest Editor
Department of Therapy and Family Medicine, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine
Interests: epstein–barr virus; Lymphadenopathy; lymphopenia; Mycobacterium tuberculosis; scrofuloderma; ace2; ifnar2; nirmatrelvir; oas1; oas3; paxlovid; disease-modifying therapy; impaired glucose tolerance; inflammatory markers; fxr; mafld; metabolism; microbiota

Special Issue Information

Dear Colleagues,

Respiratory viruses such as SARS-CoV-2, influenza viruses, and respiratory syncytial virus (RSV) cause significant acute morbidity and, in many cases, lead to persistent post-viral syndromes. These include long COVID and analogous conditions characterized by fatigue, cognitive dysfunction, respiratory issues, cardiovascular complications, and neuropsychiatric symptoms. The underlying virological mechanisms include viral persistence, immune dysregulation, autoimmunity, microvascular abnormalities, and the potential reactivation of latent viruses. Emerging research has also highlighted the role of nutritional factors, including dietary patterns and micronutrients, in modulating immune responses, reducing inflammation, and supporting recovery. This Special Issue will feature original research articles, reviews, and short communications addressing epidemiology, pathogenesis, host–virus interactions, diagnostic tools, therapeutic interventions (including pharmacological and non-pharmacological approaches), and management strategies—such as dietary and lifestyle interventions—in post-viral syndromes associated with respiratory viruses. By encompassing a broader range of viruses and interdisciplinary perspectives, including nutrition and rehabilitation, we will elucidate shared mechanisms and virus-specific features to help advance prevention, treatment, and long-term care for affected individuals.

Prof. Dr. Oleksandr Kamyshnyi
Dr. Pavlo Petakh
Dr. Iryna Halabitska
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • post-viral syndromes
  • long COVID
  • respiratory viruses
  • viral persistence
  • immune dysregulation
  • influenza
  • RSV
  • therapeutic interventions
  • nutritional strategies
  • dietary management

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Published Papers (2 papers)

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Research

10 pages, 326 KB  
Article
High Frequency of HHV-7 Reactivation in Neurological and Neuropsychiatric Long COVID: A Retrospective Observational Study
by Diane Ducret and Tatjana Mijatovic
Viruses 2026, 18(9), 1043; https://doi.org/10.3390/v18091043 (registering DOI) - 20 Sep 2026
Abstract
The neurological and neuropsychiatric manifestations of long COVID remain incompletely understood. Reactivation of latent herpesviruses has been proposed as a contributing mechanism, but human herpesvirus 7 (HHV-7) has received limited attention despite its neurotropic potential. We conducted a retrospective analysis of HHV-7 polymerase [...] Read more.
The neurological and neuropsychiatric manifestations of long COVID remain incompletely understood. Reactivation of latent herpesviruses has been proposed as a contributing mechanism, but human herpesvirus 7 (HHV-7) has received limited attention despite its neurotropic potential. We conducted a retrospective analysis of HHV-7 polymerase chain reaction (PCR) results in 30 patients (18 women and 12 men; age range, 21–55 years) with a neurological/neuropsychiatric long COVID phenotype tested within 24 months of SARS-CoV-2 infection at R.E.D. Laboratories SA, Belgium. HHV-7 positivity was compared with a historical pre-COVID-19 laboratory reference cohort comprising 320 diagnostic tests performed from 2012 to 2019. HHV-7 positivity was 29.1% (93/320; 95% CI, 24.4–34.3%) in the historical reference cohort and 76.7% (23/30; 95% CI, 59.1–88.2%) in the neurological/neuropsychiatric long COVID cohort. The between-cohort difference was significant using a two-sided Fisher’s exact test (p < 0.000001). All six patients tested within the first 12 months were HHV-7-positive. HHV-7-positive patients frequently reported neuropsychiatric symptoms, and in one longitudinal index case, viral load tracked self-reported symptom severity. In this patient-initiated retrospective study, HHV-7 positivity was substantially more frequent in the long COVID cohort than in the historical reference cohort. These findings are hypothesis-generating and support prospective investigation of HHV-7 in neurological and neuropsychiatric long COVID. Full article
(This article belongs to the Special Issue Post-Viral Syndromes Following Respiratory Virus Infections: Virological Mechanisms, Therapeutic Approaches, and Long-Term Management)
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19 pages, 3725 KB  
Article
SARS-CoV-2 N Protein Hijacks the m6A Reader YTHDF2 to Suppress Antiviral Gene Expression
by Peihan Wu, Shuai Wang and Xu Li
Viruses 2026, 18(5), 496; https://doi.org/10.3390/v18050496 - 24 Apr 2026
Viewed by 1485
Abstract
The m6A RNA methylation pathway plays a critical role in host antiviral defense. Host cells employ m6A readers such as YTHDF2 to regulate viral RNA fate through diverse mechanisms, including degradation, translational control, and immune recognition. However, we found [...] Read more.
The m6A RNA methylation pathway plays a critical role in host antiviral defense. Host cells employ m6A readers such as YTHDF2 to regulate viral RNA fate through diverse mechanisms, including degradation, translational control, and immune recognition. However, we found that YTHDF2 is essential for SARS-CoV-2 replication, suggesting that a virus may exploit this host machinery to its advantage. Through integrative RNA-proteome analysis, we identified the SARS-CoV-2 nucleocapsid (N) transcript as the most heavily m6A-modified viral transcript and a direct interactor of YTHDF2. The N protein forms a complex with YTHDF2 in the cytoplasm and redirects this host RNA decay machinery toward host antiviral transcripts. N suppresses ISG15, IFIT1, MX1 and pro-inflammatory cytokines in a largely YTHDF2-dependent manner, an effect that is lost in YTHDF2-knockout cells. These findings reveal a viral immune evasion strategy wherein a viral protein actively hijacks an m6A reader to silence antiviral gene expression, establishing the N-YTHDF2 axis as a therapeutic target against SARS-CoV-2 and other coronaviruses. Full article
(This article belongs to the Special Issue Post-Viral Syndromes Following Respiratory Virus Infections: Virological Mechanisms, Therapeutic Approaches, and Long-Term Management)
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