Human rhinoviruses (RVs) are the leading cause of the common cold and among the most prevalent infectious agents affecting humans worldwide. Although RV infections of the upper respiratory tract are generally mild and self-limiting, accumulating evidence demonstrates that RVs can contribute to substantial morbidity beyond uncomplicated cold symptoms. RV infections are increasingly recognized as important triggers of asthma and chronic obstructive pulmonary disease exacerbations, severe lower respiratory tract infections in vulnerable populations, and secondary bacterial infections. Despite their clinical relevance, the molecular and immunological mechanisms underlying RV-associated complications remain incompletely understood. Like many successful pathogens, RVs have evolved multiple strategies to modulate and evade host immune responses. Advances in virology, immunology, and omics-based technologies have substantially improved our understanding of RV–host interactions, including viral interference with innate immune signaling pathways, epithelial barrier function, interferon responses, adaptive immunity and cell metabolism. In this review, we summarize current knowledge regarding the immune evasion and immunomodulatory mechanisms employed by RVs and discuss how these processes may contribute to altered immune competence and disease pathogenesis in humans.
Peste des petits ruminants (PPR) is a highly contagious disease caused by the PPR virus (PPRV), a Morbillivirus, that affects small domestic ruminants and a range of wild ruminants. The disease is associated with significant socioeconomic losses and poses conservation threats due to its impact on susceptible wild ungulates. Wild species do not typically serve as independent reservoirs of PPRV. However, spillover from infected livestock at the wildlife–livestock interface is well documented. Therefore, understanding the role of wildlife in PPR epidemiology is important for the global campaign to eradicate the disease. This is the first large-scale surveillance of wild ruminants conducted across the Russian Federation, which included many species that were not previously tested for PPRV. In total, 1709 samples were collected from 19 wild species over 7 years (2018–2024) across 54 regions. All samples were examined using the enzyme-linked immunosorbent assay (ELISA), real-time reverse transcription–polymerase chain reaction, and virus neutralization test (VNT). For the serological component of the study, an indirect ELISA was developed, based on recombinant nucleocapsid protein expressed in Escherichia coli, and was validated. The ELISA was validated against commercial competition ELISA and VNT. Results showed that the ELISA exhibited high performance with serum from multiple species, with a sensitivity of 97.5% and a specificity of 98% compared with the commercial kit, and with a sensitivity of 96.5% and a specificity of 99% versus VNT. All 1709 wildlife samples tested negative for PPRV antibodies and RNA, indicating no evidence of viral circulation in the surveyed populations. Although PPRV has been detected in goitered gazelle (Gazella subgutturosa), saiga (Saiga tatarica), and wild goat (Capra aegagrus) in neighboring countries, none of the Russian specimens—collected from several species, including Caspian red deer (Cervus elaphus maral) and Siberian musk deer (Moschus moschiferus)—tested positive. To the best of our knowledge, this is the first reported widescale PPR surveillance in wildlife species of its kind. This first comprehensive nationwide surveillance of PPRV in wild ruminants across Russia found no infection in the species or samples tested. The newly developed ELISA offers a rapid and reliable cost-effective alternative to VNT for large-scale screening. Our findings indicate that wild ruminants do not currently serve as a PPR reservoir in the surveyed regions and support the inclusion of wildlife monitoring in PPR control strategies for a better understanding of PPR epidemiology in wildlife.
Blood-borne viral infections remain important public health concerns worldwide. Hepatitis B virus (HBV) and hepatitis C virus (HCV) are well-established transfusion-transmissible pathogens, whereas the epidemiological significance of detecting herpes simplex virus (HSV) DNA in peripheral blood remains unclear. This cross-sectional study investigated HBsAg, anti-HCV antibodies, and HSV-1/HSV-2 DNA in a community-based population in northern Thailand. Serum samples from 779 participants were tested for HBsAg and anti-HCV using rapid immunochromatographic assays, while whole-blood samples from 639 participants were tested for HSV-1 and HSV-2 DNA using real-time PCR. HBsAg and anti-HCV were detected in 3.0% (23/779) and 1.8% (14/779) of participants, respectively. HSV-1 and HSV-2 DNA were each detected in 0.5% (3/639) of whole-blood samples. In the regression analysis, higher body weight was associated with lower odds of HBsAg detection (AOR = 0.955, 95% CI: 0.929–0.982; p = 0.001). These findings provide updated community-based epidemiological data on HBV, HCV, and HSV in northern Thailand. Because HSV DNA was detected infrequently and sequence confirmation was limited, the HSV findings should be interpreted with caution. Further studies involving larger populations, quantitative viral-load measurements, and longitudinal sampling are needed.
The emergence of clade 2.3.4.4b highly pathogenic H5N1 has led to unprecedented mortality events in crane populations globally. Despite increasing concern, little is known about the prevalence of influenza A virus (IAV) and resulting antibodies in Sandhill Cranes (Antigone canadensis). To address this knowledge gap, we sampled 31 Greater and two Lesser Sandhill Cranes (Antigone canadensis tabida and Antigone canadensis canadensis, respectively) wintering in California’s Central Valley during the 2023–2024 and 2024–2025 seasons to assess active infection with IAV. None of the sampled individuals tested positive for infection with IAV via rRT-qPCR. We also sampled 29 Greater and two Lesser Sandhill Cranes for serological evidence of prior exposure to IAV; four Greater Sandhill Cranes tested positive for IAV antibodies via bELISA and antibodies specific to H5 were detected in two individuals. These findings suggest prior exposure, potentially on breeding grounds where crane mortalities related to highly pathogenic H5 have been documented. However, the low seroprevalence observed in this study suggests that the Staten Island, California, wintering population may remain largely vulnerable to future outbreaks, though small sample size does limit the broader applicability of these findings.
Early stages of host–virus interactions in peripheral tissues, such as the liver, are critical yet understudied determinants of alphavirus pathogenesis. We utilized a liver organ-on-a-chip (OOC) model consisting of primary human hepatocytes (PHHs) and Kupffer cells (KCs) to enable time-resolved tracking of Venezuelan equine encephalitis virus vaccine strain TC-83 (VEEV TC-83) replication kinetics, tissue damage, and host immunopathology. This platform was employed to evaluate the host-directed therapeutic Omaveloxolone (OMA), a known nuclear factor erythroid 2-related factor 2 (Nrf2) activator. Productive VEEV infection induced acute liver injury, indicated by parallel increases in supernatant alanine aminotransferase (ALT) and lactate dehydrogenase (LDH), alongside the newly identified pathogen-associated biomarkers γ-enolase (ENO2) and complement factor H-related protein 3 (CFHR3). Post-infection treatment with OMA within a nontoxic range altered inflammatory responses and modestly reduced viral load during the early stages, although this inhibitory efficacy was lost at later time points. Collectively, this OOC model enables the investigation of organ-specific events, demonstrating that peripheral liver responses to VEEV involve coordinated inflammatory and proteomic alterations that culminate in acute liver injury, potentially contributing to systemic inflammation and overall alphavirus disease severity.
