Chikungunya (CHIKV) and Zika (ZIKV) viruses, both mosquito-borne, often circulate simultaneously, raising concerns about the effects of coinfection. This study evaluated cytokines, chemokines, and growth factors in 12 patients with concurrent CHIKV and ZIKV infections confirmed by RT-qPCR. Clinical data and 45 immune mediators were analyzed. Coinfected and monoinfected patients exhibited similar symptoms, although ZIKV-infected individuals experienced fewer instances of fever. No patients had persistent symptoms or required hospitalization. Chemokines CCL5, CXCL1, and CXCL10 were elevated across all groups. CHIKV-infected patients showed higher levels of CCL2, CCL4, EGF, CXCL12, and IFN-α compared to controls, while IL-1RA, IL-8, and IFN-γ were elevated in both CHIKV and coinfected groups. SCF was elevated only in the ZIKV group. Overall, CHIKV and ZIKV coinfection presented mild clinical symptoms similar to monoinfections and demonstrated a moderate inflammatory response.

Lethal synergistic infections by concurrent pathogens have occurred in humans, including human immunodeficiency virus and Mycobacterium tuberculosis infections, or in animal or human models of influenza virus, or bacteria, e.g., Streptococcus pneumoniae, concurrent with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, the intracellular synergistic interaction possibilities between two respiratory viral pathogens, or between viral and fungal pathogens, merits additional examination. The requirements for synergistic concurrent pathogen infections are: a) relatively little detrimental interference between two pathogens, b) one pathogen having the capability of directly or indirectly assisting the second pathogen by direct immuno-manipulation or indirect provision of infection opportunities and/or metabolic assistance, c) substantial human or environmental prevalence, possibly including a prevalence in any type of health-care facilities or other locations having congregations of potentially infected human or animal vectors and d) substantial transmissibility of the pathogens, which would make their concurrent pathogen infections much more probable. A new definition of pathogen synergy is proposed: "pathogen synergy is an interaction of two or more pathogens during concurrent infections causing an increased infection severity compared to mono-infections by the individual pathogens." Non-respiratory pathogens can also concurrently infect organs besides the lungs. However, the air-transmissible respiratory pathogens, particularly the RNA viruses, can enable highly widespread and synergistic concurrent infections. For instance, certain strains of coronaviruses, influenza viruses and similar respiratory viruses, are highly transmissible and/or widely prevalent in various vectors for transmission to humans and have numerous capabilities for altering lung immune defenses.

Respiratory viral co-infections present significant challenges in clinical settings due to their impact on disease severity and patient outcomes. Current diagnostic methods often miss these co-infections, complicating the epidemiology and management of these cases. Research, primarily conducted in vitro and in vivo, suggests that co-infections can lead to more severe illnesses, increased hospitalization rates, and greater healthcare utilization, especially in high-risk groups such as children, the elderly, and immunocompromised individuals. Common co-infection patterns, risk factors, and their impact on disease dynamics highlight the need for advanced diagnostic techniques and tailored therapeutic strategies. Understanding the virological interactions and immune response modulation during co-infections is crucial for developing effective public health interventions and improving patient outcomes. Future research should focus on the molecular mechanisms of co-infection and the development of specific therapies to mitigate the adverse effects of these complex infections.

Explaining the evolution of cooperation in the strong altruism scenario, where a cooperator does not benefit from her contribution to the public goods, is a challenging problem that requires positive assortment among cooperators (i.e., cooperators must tend to associate with other cooperators) or punishment of defectors. The need for these drastic measures stems from the analysis of a group selection model of temporarily formed random groups introduced by Hamilton nearly fifty years ago to describe the fate of altruistic behavior in a population. Challenging conventional wisdom, we show analytically here that strong altruism evolves in Hamilton's original model in the case of biparental sexual reproduction. Moreover, when the cost of cooperation is small and the amplified contribution shared by group members is large, cooperation is the only stable strategy in equilibrium. Thus, our results provide a solution to the 'problem of origination' of strong altruism, i.e. how cooperation can take off from an initial low frequency of cooperators. We discuss a possible reassessment of cooperation in cases of viral co-infection, as cooperation may even be favored in situations where the prisoner's dilemma applies.

Avian orthoreoviruses (ARV) are an emerging threat for the poultry industry, both in the United States (US) and globally. ARV infections in turkeys have been associated with arthritis, lameness and neurological disorders, and cost the US economy approximately USD 33 million per year. There is not a commercial vaccine available and the shortage of turkey ARV (TRV) genomic data hinders the efforts to explore the molecular epidemiology of this virus, although several studies suggest a close relationship between European TRVs and TRVs present in the US. This study shows a snapshot of the genomic diversity of Avian orthoreoviruses (ARV) circulating in Germany in the mid-2000s. Through a deep genomic analysis of 18 ARV isolates recovered from sick turkeys, we observed that co-infection was a common condition. 80% of the samples showed signs of a simultaneous infection with a TRV and a chicken ARV (CRV). We believe this is the first reported evidence of CRV and TRV naturally occurring co-infections in commercial turkeys. These co-infection events were identified due to the significant genomic diversity observed among ARV infecting various production bird species. Our phylogenetic analysis revealed a consistent host-associated ARV clustering, with three main clades: (i) a TRV clade, (ii) a CRV clade, and (iii) a Duck ARV (DRV)/Goose ARV (GRV) clade. Furthermore, our findings indicate that German TRVs have interacted with their European and American counterparts, suggesting active mobilization of the virus, likely through the commercial trading of live animals. However, we also consider the potential role of migratory birds in the international movement of ARV.

The growing urbanization process is accompanied by the emergence of new habitats for wildlife, and cities are sometimes seen as refuges for pollinators such as wild bees compared to intensively cultivated rural habitats. However, the contrasting living conditions that combine high fragmentation, exposure to pollutants, and heat island effects, with low pesticide use and potentially high availability of resources, make it difficult to predict the overall effect of urban living on the health of wild bees. Moreover, if the responses of wild bee populations in terms of species richness and diversity have been the focus of many recent studies, individual responses to urbanization have been more rarely investigated. More specifically, data on the impacts on individual bee physiology and health are lacking. To help fill this gap, we collected red-tailed bumblebee (Bombus lapidarius) workers along a gradient of urbanization defined by the level of soil imperviousness, and estimated environmental (air quality) and ecological (pathogens' prevalence and loads; local competition) pressures they locally experienced. In parallel, we quantified the expression of selected immune marker genes. We measured how the immune system of bumblebees responds to urbanization gradient and which local parameters best explain the observed changes in immune gene expression. We evidenced three immune markers, tightly linked with cellular metabolism, whose expressions increase with the level of urbanization, independently of individual infection and pollution exposure. We suggest that induction of their expression reveals a shift in wild bee immunometabolism, supposedly in response to the stressful conditions experienced in areas with high built-up cover. The induction of these genes is likely at the root of any immune activation; they could thus be used as markers to estimate the levels of urban stress locally experienced by pollinators.

This study aimed to analyze the epidemic characteristics and influencing factors of school influenza outbreaks in Jiangsu Province, China from 2020 to 2023,following the COVID-19 pandemic, to inform prevention and control strategies.

Data on influenza-like illness(ILI) outbreaks from the Chinese Influenza Surveillance Information System and national-level influenza surveillance sentinel hospitals were analyzed. The temporal distribution, school type, virus strains, and outbreak scales were examined using descriptive statistics.

From 2020 to 2023, 1142 influenza outbreaks occurred in schools, with primary schools(ages 6 to 12) accounting for 71.80%. Most large outbreaks were caused by A(H1N1) and A(H3N2), responsible for 8.99% of total outbreaks. Outbreaks were predominantly reported in the pre-peak periods of B(Victoria) and A(H1N1) circulation, accounting for 86.31% and 92.32% of their respective total outbreaks. No concurrent influenza and COVID-19 outbreaks were observed during the study period.

Primary and secondary schools are high-risk settings for influenza outbreaks. A(H3N2) shows higher adaptability and is more likely to co-circulate with other subtypes/lineages, especially A(H1N1), leading to larger outbreaks. B(Victoria)-caused outbreaks are more frequent but smaller in scale. School influenza outbreaks are more likely to occur during the early stages of seasonal peaks, particularly for B(Victoria) and A(H1N1). This suggests that influenza outbreaks in schools may play a crucial role in seeding and accelerating the spread of the virus within the broader community.

Respiratory viruses are known to represent a high burden in winter, yet the seasonality of many viruses remains poorly understood. Better knowledge of co-circulation and interaction between viruses is critical to prevention and management. We use > 10-year active surveillance in the Valencia Region to assess seasonality and co-circulation.

Over 2010-2021, samples from patients hospitalised for acute respiratory illness were analysed using multiplex real-time PCR to test for 9 viruses: influenza, respiratory syncytial virus (RSV), parainfluenza virus (PIV), rhino/enteroviruses (HRV/ENV), metapneumovirus (MPV), bocavirus, adenovirus, SARS-CoV-2 and non-SARS coronaviruses (HCoV). Winter seasonal patterns of incidence were examined. Instances of co-detection of multiple viruses in a sample were analysed and compared with expected values under a crude model of independent circulation.

Most viruses exhibited consistent patterns between years. Specifically, RSV and influenza seasons were clearly defined, peaking in December-February, as did HCoV and SARS-CoV-2. MPV, PIV and HRV/ENV showed less clear seasonality, with circulation outside the observed period. All viruses circulated in January, suggesting any pair had opportunity for co-infection. Multiple viruses were found in 4% of patients, with more common co-detection in children under 5 (9%) than older ages. Influenza co-detection was generally observed infrequently relative to expectation, while RSV co-detections were more common, particularly among young children.

We identify characteristic patterns of viruses associated with acute respiratory hospitalisation during winter. Simultaneous circulation permits extensive co-detection of viruses, particularly in young children. However, virus combinations appear to differ in their rates of co-detection, meriting further study.

Epizootic hemorrhagic disease (EHD), caused by Epizootic hemorrhagic disease virus (EHDV), is an emerging and severe livestock disease. Recent incursion and distribution of EHDV in Europe have outlined the emerging character of EHD. Despite its worldwide impact, numerous knowledge gaps exist. A range of inconveniences restricts utilization of natural hosts of EHDV. Here, we show that adult mice deficient in type I IFN receptor (IFNAR(-/-)) are highly susceptible to EHDV-6 and EHDV-8 infection when the virus is administered subcutaneously. Disease was characterized by ruffled hair, reluctance to move, dehydration and conjunctivitis, with viraemia detected from day 5 post-infection. A deeper characterization of EHDV-8 infection showed viral replication in the lung, liver, spleen, kidney, testis and ovaries. Importantly, increased expression levels of pro-inflammatory cytokines IL-1β, IL-6 and CXCL2 were observed in spleen after EHDV-8 infection. Furthermore, IFNAR(-/-) adult mice immunized with a EHDV-8 inactivated vaccine elicited neutralizing antibodies specific of EHDV-8 and full protection against challenge with a lethal dose of this virus. This study also explores the possibilities of this animal model for study of BTV and EHDV coinfection. In summary, the IFNAR(-/-) mouse model faithfully recapitulates EHD and can be applied for vaccine testing, which can facilitate progress in addressing the animal health challenge posed by this virus.

Viral co-infections are frequently observed among children, but whether specific viral interactions enhance or diminish the severity of respiratory disease is still controversial. This study aimed to investigate the type of viral mono- and co-infections by also evaluating viral correlations in 3525 respiratory samples from 3525 pediatric in/outpatients screened by the Allplex Respiratory Panel Assays and with a Severe Acute Respiratory Syndrome-COronaVirus 2 (SARS-CoV-2) test available. Overall, viral co-infections were detected in 37.8% of patients and were more frequently observed in specimens from children with lower respiratory tract infections compared to those with upper respiratory tract infections (47.1% vs. 36.0%, p = 0.003). SARS-CoV-2 and influenza A were more commonly detected in mono-infections, whereas human bocavirus showed the highest co-infection rate (87.8% in co-infection). After analyzing viral pairings using Spearman's correlation test, it was noted that SARS-CoV-2 was negatively associated with all other respiratory viruses, whereas a markedly significant positive correlation (p < 0.001) was observed for five viral pairings (involving adenovirus/human bocavirus/human enterovirus/metapneumoviruses/rhinovirus). The correlation between co-infection and clinical outcome may be linked to the type of virus(es) involved in the co-infection rather than simple co-presence. Further studies dedicated to this important point are needed, since it has obvious implications from a diagnostic and clinical point of view.

A massive mortality event concerning farmed Chinese tongue soles occurred in Tianjin, China, and the causative agent remains unknown. Here, a novel Cynoglossus semilaevis papillomavirus (CsPaV) and parvovirus (CsPV) were simultaneously isolated and identified from diseased fish via electron microscopy, virus isolation, genome sequencing, experimental challenges, and fluorescence in situ hybridization (FISH). Electron microscopy showed large numbers of virus particles present in the tissues of diseased fish. Viruses that were isolated and propagated in flounder gill cells (FG) induced typical cytopathic effects (CPE). The cumulative mortality of fish given intraperitoneal injections reached 100% at 7 dpi. The complete genomes of CsPaV and CsPV comprised 5939 bp and 3663 bp, respectively, and the genomes shared no nucleotide sequence similarities with other viruses. Phylogenetic analysis based on the L1 and NS1 protein sequences revealed that CsPaV and CsPV were novel members of the Papillomaviridae and Parvoviridae families. The FISH results showed positive signals in the spleen tissues of infected fish, and both viruses could co-infect single cells. This study represents the first report where novel papillomavirus and parvovirus are identified in farmed marine cultured fish, and it provides a basis for further studies on the prevention and treatment of emerging viral diseases.

Co-infection or superinfection of the host by two or more virus species is a common event, potentially leading to viral interference, viral synergy, or neutral interaction. The simultaneous presence of two or more viruses, even distantly related, within the same cell depends upon viral tropism, i.e., the entry of viruses via receptors present on the same cell type. Subsequently, productive infection depends on the ability of these viruses to replicate efficiently in the same cellular environment. HIV-1 initially targets CCR5-expressing tissue memory CD4+ T cells, and in the absence of early cART initiation, a co-receptor switch may occur, leading to the infection of naïve and memory CXCR4-expressing CD4+ T cells. HIV-1 infection of macrophages at the G1 stage of their cell cycle also occurs in vivo, broadening the possible occurrence of co-infections between HIV-1 and other viruses at the cellular level. Moreover, HIV-1-infected DCs can transfer the virus to CD4+ T cells via trans-infection. This review focuses on the description of reported co-infections within the same cell between HIV-1 and other human pathogenic, non-pathogenic, or low-pathogenic viruses, including HIV-2, HTLV, HSV, HHV-6/-7, GBV-C, Dengue, and Ebola viruses, also discussing the possible reciprocal interactions in terms of virus replication and virus pseudotyping.

Microorganisms, especially viruses, cause disease in both humans and animals. Environmental chemical pollutants including microplastics, pesticides, antibiotics sand air pollutants arisen from human activities affect both animal and human health. This review assesses the impact of chemical and biological contaminants (virus and bacteria) on viruses including its life cycle, survival, mutations, loads and titers, shedding, transmission, infection, re-assortment, interference, abundance, viral transfer between cells, and the susceptibility of the host to viruses. It summarizes the sources of environmental contaminants, interactions between contaminants and viruses, and methods used to mitigate such interactions. Overall, this review provides a perspective of environmentally co-occurring contaminants on animal viruses that would be useful for future research on virus-animal-human-ecosystem harmony studies to safeguard human and animal health.

Since the first case of COVID-19 was diagnosed in Wuhan, China in late 2019, concomitant infections with Herpesviridae were documented that were presented from simple skin manifestations to severe life-threatening conditions that may lead to mortality. In this systematic review, we have included studies conducted in different parts of the world to find out the association of clinical features and outcomes of COVID-19 infection and concomitant Herpesviridae infection.

A comprehensive search was conducted in electronic databases including Medline through PubMed, Cochrane database, Scopus and Web of science (core collection). Two review authors independently screened the articles and extracted data. The Risk of bias assessment was done by using RoBANS tool.

A total of 919 studies were retrieved and 19 studies were included having data of 539 patients who were infected with both COVID-19 and Herpesviridae. Herpes Simplex-1, Varicella Zoster, Cytomegalovirus, Epstein-Barr virus and Human Herpes Virus-6 were the detected viruses in the included studies. Cytomegalovirus (CMV) reactivation was the most detected concomitant infection. In case of reactivation with more than one Herpes virus mortality among patients were detected along with single viral infection in some studies. Significant association was noted in dosage and usage of steroid and Herpesviridae reactivation in COVID-19 patients. Blood markers such as D-dimer, CRP along with length of stay in the ICU and usage of invasive mechanical ventilation were found to be the significantly associated markers.

Findings from this study will aid clinicians to assess and treat COVID-19 cases with co-infections.

Complex virus-virus interactions can arise when multiple viruses coinfect the same host, impacting infection outcomes with broader ecological and evolutionary significance for viruses and host. Yet, our knowledge regarding virus competition is still limited, especially for single-celled eukaryotic host-virus systems. Here, we report on mutual interference of two dsDNA viruses, MpoV-45T and MpoV-46T, competing for their Arctic algal host Micromonas polaris. Both viruses affected each other's gene expression and displayed reduced genome replication during coinfection. MpoV-45T was the dominant virus, likely due to interference in the DNA replication of is competitor. Even when its coinfection was delayed, the dominant virus still prevailed while genome production of the other virus was strongly suppressed. This contrasts with typical superinfection exclusion, where the primary infection prevents secondary infection by other viruses. Higher temperature made the suppressed virus a stronger competitor, signifying that global warming is likely to alter virus-virus interactions in Arctic waters.