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Emerging Viral Epidemics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 2151

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Guest Editor
National and Kapodistrian University of Athens, School of Medicine, Clinical Microbiology Laboratory, ATTIKON University Hospital, Athens, Greece
Interests: molecular virology; COVID; SARS-CoV-2
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Special Issue Information

Dear Colleagues,

Emerging viral epidemics and pandemics result from the complex interaction between viral evolution and human activity. The exceptionally high genetic diversity exhibited by some viruses, particularly those with an RNA genome, confers significant evolutionary potential, which may lead to the emergence of antigenically novel strains with increased virulence and transmissibility. Conversely, ecosystem changes driven by environmental destruction and deforestation, poverty, war, social unrest, inadequate social policies in many countries, population movements, animal migration due to environmental changes, weaknesses in public health systems, mass transportation, and overcrowding in large cities are key anthropogenic factors that significantly contribute to the emergence of severe epidemics and pandemics. Therefore, human civilization is perpetually at risk of facing a serious epidemic or pandemic.

Addressing emerging viral epidemics requires multidisciplinary approaches that encompass advancements in diagnostics, epidemiology, pathophysiology, surveillance, and public health infrastructure. This Special Issue of the International Journal of Molecular Sciences aims to provide further insight into the challenges posed by emerging viral epidemics and pandemics, as well as to highlight the lessons that we have learned from recent devastating epidemics.

Dr. Nikolaos Siafakas
Guest Editor

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Keywords

  • emerging viruses
  • diagnostic virology
  • viral epidemiology
  • viral evolution
  • zoonotic infections
  • public health
  • surveillance

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Published Papers (2 papers)

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15 pages, 1721 KB  
Article
Assessing Seroprevalence and Infection Dynamics of Oncogenic Gammaherpesviruses in South African Paediatric Patients Presenting with Inflammatory Conditions
by Katrin Bratl, Claire Butters, Kate Webb and Georgia Schäfer
Int. J. Mol. Sci. 2026, 27(3), 1275; https://doi.org/10.3390/ijms27031275 - 27 Jan 2026
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Abstract
Kaposi’s Sarcoma-associated herpesvirus (KSHV) and Epstein–Barr virus (EBV) are oncogenic gammaherpesviruses with high prevalence in sub-Saharan Africa. Both viruses are typically acquired during childhood, establishing lifelong latency. While viral reactivation into the lytic cycle has been mainly studied in adult HIV-infected populations—and more [...] Read more.
Kaposi’s Sarcoma-associated herpesvirus (KSHV) and Epstein–Barr virus (EBV) are oncogenic gammaherpesviruses with high prevalence in sub-Saharan Africa. Both viruses are typically acquired during childhood, establishing lifelong latency. While viral reactivation into the lytic cycle has been mainly studied in adult HIV-infected populations—and more recently in the context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) co-infection—the dynamics of KSHV and EBV infection in children remain poorly understood. Here, we characterize pediatric patients (n = 175; median age 4.6 years; IQR 2.0–8.3) presenting with inflammatory conditions during the COVID-19 pandemic in South Africa (from July 2020 to February 2024). Including a healthy, non-inflammatory control group, we found widespread exposure to SARS-CoV-2 (70.9% seropositivity), with 72.6% of the children being seropositive for EBV and 19.4% for KSHV. There were no significant differences in seroprevalence between children with inflammatory conditions and healthy controls for any of these viruses, although SARS-CoV-2 antibody titers were significantly higher in the inflammatory group, while EBV immune responses were lower in children presenting with inflammation. Among the KSHV-seropositive children, no active viremia was detected (as determined by the absence of viral DNA in the peripheral blood). In contrast, 34.4% of EBV-seropositive children had detectable EBV viral load, with a modestly higher proportion in the inflammatory group. However, EBV viral load levels were comparable between children diagnosed with Multisystem Inflammatory Syndrome in Children (MIS-C), Kawasaki Disease (KD), and other inflammatory conditions. Logistic regression analyses revealed that increasing age was significantly associated with higher risk of SARS-CoV-2 and EBV seropositivity, but not KSHV. Notably, the risk of EBV DNA detection in the peripheral blood decreased with age. In summary, this study suggests effective immunological control of gammaherpesvirus infections in HIV-negative paediatric patients, even in the presence of inflammatory conditions that might otherwise trigger viral reactivation. Full article
(This article belongs to the Special Issue Emerging Viral Epidemics)
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13 pages, 752 KB  
Brief Report
Retrospective Observational Study of CSF-Derived HIV-1 Tat and Vpr Amino Acid Sequences in a South African Pediatric Cohort with HIV Subtype C
by Anicia Thirion, Shayne Mason, Du Toit Loots, Regan Solomons and Monray Edward Williams
Int. J. Mol. Sci. 2025, 26(11), 5008; https://doi.org/10.3390/ijms26115008 - 22 May 2025
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Abstract
The human immunodeficiency virus (HIV-1) infiltrates the central nervous system (CNS) early in infection, leading to HIV-associated neurocognitive impairments, particularly pronounced in children who exhibit neurodevelopmental delay. Viral proteins, including the transactivator of transcription protein (Tat) and viral protein R (Vpr) are pivotal [...] Read more.
The human immunodeficiency virus (HIV-1) infiltrates the central nervous system (CNS) early in infection, leading to HIV-associated neurocognitive impairments, particularly pronounced in children who exhibit neurodevelopmental delay. Viral proteins, including the transactivator of transcription protein (Tat) and viral protein R (Vpr) are pivotal in HIV-1 neuropathogenesis, with their amino acid sequence variation influencing disease progression. Due to the difficulty of collecting cerebrospinal fluid from children, few studies have examined whether key Tat and Vpr neuropathogenic signatures found in blood are also present in the cerebrospinal fluid (CSF) of children with HIV. We employed Sanger sequencing for Tat and Vpr sequence analysis using retrospectively collected CSF samples from a South African pediatric HIV-1 subtype C cohort (n = 4). We compared our CSF-derived sequences with pediatric blood-derived sequences (n = 43) from various geographical regions, sourced from the Los Alamos database. Neuropathogenic amino acid variants were identified in Tat and Vpr sequences derived from CSF samples of South African pediatric participants No significant differences were found between subtype C sequences from CSF and blood. Regional analysis highlighted unique amino acid signatures. Obtaining pediatric CSF for HIV-1 sequencing is highly challenging. Despite a small sample size, this study offers rare insights into Tat and Vpr sequences in children, improving understanding of the potential HIV-1 brain pathogenesis in pediatric populations. Full article
(This article belongs to the Special Issue Emerging Viral Epidemics)
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