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PubMed2026

An enhanced multisegment RT-PCR method for influenza A virus sequencing: Improved performance and reduced preparation time over traditional methods.

Influenza A viruses (IAVs) remain a major global health threat, affecting both human and animal populations. Whole-genome sequencing is essential for monitoring viral evolution, zoonotic transmission, and emerging variants. However, conventional RT-PCR methods often result in incomplete gene coverage, amplification biases, and reduced sequencing accuracy, particularly in clinical samples. We developed a robust In-house method for IAV full-genome sequencing using the Oxford Nanopore Technologies (ONT) long-read sequencing platform. This method integrates an in-house multisegment Reverse Transcription PCR (RT-PCR) method with a streamlined 2-pool primer design targeting all eight IAV gene segments. RNA extracted from clinical and stock virus samples was reverse-transcribed and amplified using Superscript IV-based chemistry, followed by magnetic bead purification to ensure high-quality amplicons. Sequencing libraries were prepared with the Native Barcoding Kit 24 (SQK-NBD114.24) and sequenced on R10.4.1 flow cells on the MinION MK1C device. Data analysis using the Iterative Refinement Meta-Assembler (IRMA) confirmed improved read depth, uniform coverage, and complete genome recovery. Compared to conventional methods, our In-House Multisegment 2-Pool (IH-MS2P) RT-PCR method generated higher numbers of matched read counts, minimized chimeric artifacts, and delivered superior genome coverage across human, swine, and avian isolates. This optimized RT-PCR method provides a high-performance, time-efficient, and portable solution for influenza genomics, demonstrating robust applicability even with clinical samples of low RNA yield.

Influenza A virus↗
PubMed2026

Endemic Circulation and Genetic Characterization of Foot-and-Mouth Disease Virus in Buffalo Populations of Bangladesh.

Foot-and-mouth disease (FMD) virus (FMDV) is endemic in Bangladesh, causing severe economic losses in the livestock sector. While it primarily affects cattle, buffaloes (Bubalus bubalis) remain highly susceptible. Therefore, this study aimed to determine the prevalence and molecular characteristics of FMDV in buffaloes across three districts (Sylhet, Rajshahi, and Noakhali) of Bangladesh from January to June 2024. In a cross-sectional study, a total of 622 nasal swabs from 67 herds were collected and tested for FMDV RNA using reverse transcription polymerase chain reaction (RT-PCR). Overall, 255 samples were positive, resulting in an individual-level prevalence of 41.0%(255/622), while 88.1% (59/67) of herds were FMDV-positive. Animal-level prevalence was highest in Sylhet (47.1%), followed by Noakhali (38.9%) and Rajshahi (37.1%). To further characterize circulating strains, eight representative RT-PCR-positive samples were sequenced, revealing the co-circulation of serotypes O (n = 5) and Asia-1 (n = 3). Phylogenetic analysis showed that the isolates belonged to the ME-SA/Ind2001e lineage of the serotype O and the Asia-1 Group V lineage, clustering with contemporary strains from Bangladesh and neighboring countries, suggesting possible intra- and transboundary transmission. Pairwise genetic distance evaluation revealed high regional similarity, while Mantel tests indicated significant associations between genetic, geographic, and temporal distances. Comparative genomic analysis revealed largely conserved genomic regions, whereas VP1 analysis indicated that purifying selection predominated across both serotypes, with serotype O exhibiting greater genetic diversity (π = 0.11642) than Asia-1 (π = 0.05258), suggesting localized antigenic variability and possible immune-mediated viral evolution. These findings highlight the need for strengthened surveillance, improved biosecurity, and integrated vaccination strategies to enhance FMD control and reduce economic losses in Bangladesh.

Animals↗
PubMed2026

A comprehensive overview of monkeypox virus disease.

BACKGROUND: Monkeypox (mpox), caused by monkeypox virus (MPXV), re-emerged as a major global public health concern in 2022, resulting in widespread transmission beyond traditionally endemic regions. As of March 2026, 181,164 confirmed cases and 492 deaths had been reported across 144 countries globally. The unprecedented geographic spread of the outbreak highlighted important knowledge gaps in disease surveillance, prevention, and control. Given the ongoing global circulation of MPXV and the risk of future outbreaks, this review provides a comprehensive synthesis of current evidence on MPXV and mpox. METHODS: The literature, surveillance data, and public health reports available up to March 2026 were systematically reviewed and synthesized. The review comprehensively assesses viral biology, genetic diversity, epidemiology, transmission dynamics, clinical manifestations, pathogenesis, laboratory diagnosis, infection during pregnancy, host immune responses, immune evasion mechanisms, therapeutic interventions, and prevention strategies. FINDINGS AND CONCLUSIONS: Globally, the decline in public immunity following the cessation of routine smallpox vaccination, together with ongoing viral evolution, may have contributed to the resurgence of mpox. Advances in genomic surveillance, diagnostics, and public health preparedness have strengthened outbreak response; however, important gaps remain in understanding long-term immunity and optimal treatment strategies. This review summarizes current evidence on MPXV and mpox and highlights priorities for future research and public health interventions.

Antiviral therapy↗
PubMed2025

Defective but tumorigenic: the evolutionary and functional roles of mutated oncoviruses.

Human oncogenic viruses contribute significantly to the global health burden and include seven types: Epstein-Barr virus, hepatitis B virus, human T-cell leukemia virus type 1, human papillomavirus, hepatitis C virus, Kaposi's sarcoma-associated herpesvirus, and Merkel cell polyomavirus. While the roles of latent or integrated viral genomes in cancer have been documented, emerging evidence highlights the contribution of defective viruses-those carrying intragenic deletions or loss-of-function mutations-in promoting viral oncogenesis. These altered genomes often lack genes essential for lytic replication or immune recognition, which enhances their persistence and immune evasion. In virus-associated diseases, specific patterns of gene retention and deletion suggest that host-driven selective pressures drive the emergence of these altered genomes. This review examines the generation, prevalence, and functional impact of these viruses, reframing them as active participants in disease development and progression. Recognizing their role offers new insights into viral tumor evolution and creates opportunities for applications in viral diagnostics and targeted intervention strategies.

Humans↗
PubMed1975

Evolution of type C viral genes: preservation of ancestral murine type C viral sequences in pig cellular DNA.

Domestic pigs (Sus scrofa) and other members of the family Suidae have multiple copies of type C viral gene sequences in the cellular DNA of all their tissues. Partially homologous viral gene sequences are also found in cellular DNA of rodents, particularly Muridae. The results lead to the conclusion that type C viral genes were introduced into the Suidae lineage as a result of trans-species infection by an ancestral xenotropic murine virus. The rate of evolution of the virogene sequences in the pig appears to be much slower than that of genes that have remained in the rodent lineage; this may be a consequence of transfer from a shorter-lived animal (the rodent) to a longer-lived one (the pig). We estimate the time of gene transmission as 5-10 million years ago and conclude that the present-day porcine type C virogenes most closely approximate the viral genes as they were several million years ago in the rodent lineage.

Animals↗
PubMed1975

Evolution of type C viral genes: origin of feline leukemia virus.

Reiterated gene sequences related to the RNA of feline leukemia virus (FeLV) are detected in all tissues of domestic cats and their close Felis relatives but not in more distantly related Felis species. Partially homologous viral gene sequences are found in rodent, and particularly rat, DNA. Together with the immunologic relationships observed between FeLV and endogenous rodent type C viruses, the results lead to the conclusion that FeLV-related genes were transmitted from a rodent to cat ancestor and have been perpetuated in the germ line of cats.

Animals↗
PubMed1976

Evolution of type C viral genes: evidence for an Asian origin of man.

Old World monkeys and apes, including man, possess, as a normal component of their cellular DNA, gene sequences (virogenes) related to the RNA of a virus isolated from baboons. A comparison of the viral gene sequences and the other cellular sequences distinguishes those Old World monkeys and apes that have evolved in Africa from those that have evolved in Asia. Among the apes, only gorilla and chimpanzee seem by these criteria to be African, whereas gibbon, orang-utan and man are identified as Asian, leading us to conclude that most of man's evolution has occurred outside Africa.

Africa↗
PubMed2027

Nanopore Sequencing for Chikungunya Virus: Principles and Application.

Nanopore sequencing is transforming viral genomics through real-time, portable, long-read analysis of RNA and DNA. Unlike traditional short-read platforms, it detects nucleotide sequences by measuring ionic current changes as nucleic acids pass through nanoscale pores, enabling direct single-molecule sequencing and base modification detection. Its simplicity, flexibility, and capacity for ultra-long reads make it ideal for resolving complex genomic regions, structural variants, and full viral genomes. These advantages have accelerated its use in pathogen surveillance and outbreak response, especially in resource-limited settings. For chikungunya virus (CHIKV), nanopore sequencing allows rapid, culture-independent recovery of complete genomes from clinical and vector samples, enabling real-time tracking of viral diversity, evolution, and spread. Experiences from Ebola, Zika, and COVID-19 have demonstrated the power of portable sequencing, now applied to CHIKV monitoring. Advances in tools such as Guppy, Dorado, Minimap2, and Medaka enhance read quality, consensus accuracy, and downstream analyses. Despite challenges in basecalling and error correction, robust quality control pipelines ensure reliable results. Ongoing improvements in chemistry, flow cell design, and machine learning will further enhance fidelity and throughput, establishing nanopore sequencing as a cornerstone of CHIKV genomic surveillance and epidemic preparedness.

Chikungunya virus↗
PubMed1979

[Use of the serum enzymes gamma-glutamyl transpeptidase and pseudocholinesterase in hepatic pathology].

Serum gammaglutamyl transpeptidase (gammaGT) and seudocholinesterase (CHE) were studied in 20 patients with acute viral hepatitis and 36 with alcoholic cirrhosis. All had from moderate to severe clinical evolution. gammaGT is an enzyme useful to determine, as to follow clinical-biochemical evolution of viral hepatitis specially in the colestatic form. CHE can be used as an evolution pointer of liver insufficiency specially in cirrhosis.

Acute Disease↗
PubMed2026

Virome-wide ubiquitin ligase discovery reveals diverse mechanisms of immune evasion.

Viruses are intracellular parasites that reprogram the host proteome to promote replication and evade immune recognition. We applied a virome-wide library of ~10,000 open reading frames to discover viral ubiquitin ligases, mapping their mechanisms of degradation and host substrates using targeted CRISPR screens and proteomics. These viral effectors could be classified as canonical ligases that mimic host E3s, hijackers that redirect host E3s, and noncanonical ligases that rewire cullin-RING ligase machinery. These diverse strategies of virus-mediated degradation converged on immune-related substrates, including JAK1 and CUL1β-TrCP, underscoring immune evasion as a major driver of viral ubiquitin ligase evolution. Our findings elucidate viral strategies for exploiting the ubiquitin-proteasome system with potential for therapeutic targeting.

Humans↗
PubMedDate not supplied

[A few viral infections in the recent epidemiological evolution (author's transl)].

In the study we presented a few infections of viral etiology that showed evident epidemiological evolutions during the last ten years. We refered of a disease nearly eradicated, of one that can be eradicated, and of a group of infections that at present cannot be eradicated. The first is poliomyelitis, the second is measles, the third is represented by viral infections connected with the respiratory tract. As for the first disease, the sistematic immunoprophilaxis applyed in different countries of the world on one hand stopped the transmission of wild polioviruses and on the other created an immunological barrier in those countries where polio vaccination is maintained, as demonstrated by statistics revealing the absence or low incidence of this disease. As for the epidemiological evolution of measles, after considering the incidence due to age, environment, social-hygienic conditions, mortality etc..., we refered in particular of a vaccination that took place in USA where the disease decreased with 1968 then rised next year a pause of the vaccination program. A second cycle of vaccinations against measles revealed in 1972 a decrease of the disease this signifying the importance of the vaccination in stopping, reducing or modifying the epidemiology of measles. The epidemiological conditions of respiratory infections are completely different due to the variety of the etiological factors, the difficulty in preparing aspecific vaccines, and the impossibility in recognising clinical forms caused by these viruses. All these factors, impede, actually, a complete eradication.

Africa↗
PubMed1992

Anatomy and evolution of proteins displaying the viral capsid jellyroll topology.

In this paper the anatomy of 25 structures containing a jellyroll motif, consisting of eight antiparallel beta-strands forming a so-called beta-barrel, was investigated. This involved performing a careful structural alignment based on hydrogen bonds for the equivalent regions of the tertiary folds and a subsequent analysis of conserved amino acids, equivalenced residue-residue contacts, and various parameters describing the size, shape and other geometrical characteristics of these regions. It was found that the jellyroll motif is best viewed as a two-sheet wedge structure rather than a barrel. The more conserved parameters are discussed. A model of evolutionary development for the jellyroll fold in the various protein and viral structures is proposed.

Amino Acid Sequence↗
PubMed2024

TMPRSS2-mediated SARS-CoV-2 uptake boosts innate immune activation, enhances cytopathology, and drives convergent virus evolution.

The accessory protease transmembrane protease serine 2 (TMPRSS2) enhances severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uptake into ACE2-expressing cells, although how increased entry impacts downstream viral and host processes remains unclear. To investigate this in more detail, we performed infection assays in engineered cells promoting ACE2-mediated entry with and without TMPRSS2 coexpression. Electron microscopy and inhibitor experiments indicated TMPRSS2-mediated cell entry was associated with increased virion internalization into endosomes, and partially dependent upon clathrin-mediated endocytosis. TMPRSS2 increased panvariant uptake efficiency and enhanced early rates of virus replication, transcription, and secretion, with variant-specific profiles observed. On the host side, transcriptional profiling confirmed the magnitude of infection-induced antiviral and proinflammatory responses were linked to uptake efficiency, with TMPRSS2-assisted entry boosting early antiviral responses. In addition, TMPRSS2-enhanced infections increased rates of cytopathology, apoptosis, and necrosis and modulated virus secretion kinetics in a variant-specific manner. On the virus side, convergent signatures of cell-uptake-dependent innate immune induction were recorded in viral genomes, manifesting as switches in dominant coupled Nsp3 residues whose frequencies were correlated to the magnitude of the cellular response to infection. Experimentally, we demonstrated that selected Nsp3 mutations conferred enhanced interferon antagonism. More broadly, we show that TMPRSS2 orthologues from evolutionarily diverse mammals facilitate panvariant enhancement of cell uptake. In summary, our study uncovers previously unreported associations, linking cell entry efficiency to innate immune activation kinetics, cell death rates, virus secretion dynamics, and convergent selection of viral mutations. These data expand our understanding of TMPRSS2's role in the SARS-CoV-2 life cycle and confirm its broader significance in zoonotic reservoirs and animal models.

SARS-CoV-2↗
PubMed1991

An evolutionary view of viral regulatory genes.

It is my great honor to dedicate this article to Professor Ludwig C. Yen at the occasion of the Annual Meeting of the Chinese Society of Microbiology, commemorating his 101st Birthday. I have had the privilege of being one of the earliest students of Professor Yen, and as a staff member working for 16 years under him, I have been benefited enormously from his teachings. I am most grateful to Dr. Czausiung Yang and the executive board members of the Chinese Society of Microbiology for giving me this opportunity to present some of my research activities which would be relevant to Professor Yen's teachings. Introduction to the evolutionary view of host-parasite relationship was one of the many contributions Professor Yen made to enlighten students and colleagues as early as in 1940. As promulgated by Professor Yen, natural history of infectious diseases has witnessed the reality of Theobald Smith's premise, "pathogenicity of microorganisms is an accident in the evolutionary processes of host-parasite relationship, and the outcome of evolutionary forces is a modus vivendi (a feasible compromise) according to which the parasite and the host reach some sort of equilibrium which permits the survival of both"(1). These evolutionary concept has since become a common knowledge for modern students of infectious diseases. The natural history of recently discovered human retroviruses such as HTLVs (human T-lymphotropic viruses) and HIVs (human immunodeficiency viruses) has amply demonstrated the truth of the premise. I shall review some results of our research which would be of relevance to the evolution of viral quasispecies and variants, viral oncogenes, and the cellular as well as viral regulatory genes. I shall focus on the roles played by these genes in the delicate and complex balance of host-virus relationships, and on their association with cellular differentiation and oncogenesis.

Biological Evolution↗
PubMed2026

The factory enters the fray: how mitochondrial protein trafficking shapes the host response to infection.

Beyond textbook functions in homeostatic metabolism, mitochondria are now recognized as central coordinators of cell-intrinsic and cell-extrinsic immune responses to infection. Directed trafficking of proteins and other molecules between mitochondria and the rest of the cell underlies a growing catalog of these activities. Some are pro-host; others are antagonized by viral effectors or co-opted by viruses entirely. How host and viral factors rewire the mitochondrial proteome during infection to shape these outcomes remains incompletely understood. The evolutionary history of this system adds another dimension: mitochondria retain biochemical signatures of their α-proteobacterial endosymbiotic origin, and ongoing co-evolution between viral, host, and mitochondrial genomes continues to shape the proteins that traffic to and from the organelle. Using published examples, we highlight general principles, mechanisms, and consequences of host and viral protein localization to and from the mitochondria. To support discovery, we present integrated gene lists identifying host mitochondrial factors with evidence for type I interferon stimulation, interactions with viral proteins, and signatures of positive selection. Together, these resources and the principles within offer a framework for understanding mitochondria not as passive metabolic machinery but as actively contested cellular territory whose protein composition is continuously negotiated between the host and the pathogen.

adaptation↗
PubMed2025

Experimental Evolution of Poxviruses.

Experimental evolution is the process of exposing virus populations to defined selective pressures in a laboratory setting to identify adaptive changes. Coupled with deep sequencing, this experimental approach allows for nucleotide-level resolution of poxvirus adaptive strategies over time. Here, we present a general method of poxvirus experimental evolution, Illumina-based deep sequencing, and bioinformatic analyses to identify structural changes (e.g., gene duplication) as well as local adaptive changes (e.g., small indels and single nucleotide polymorphisms).

Poxviridae↗
PubMed1992

New aspects of influenza viruses.

Influenza virus infections continue to cause substantial morbidity and mortality with a worldwide social and economic impact. The past five years have seen dramatic advances in our understanding of viral replication, evolution, and antigenic variation. Genetic analyses have clarified relationships between human and animal influenza virus strains, demonstrating the potential for the appearance of new pandemic reassortants as hemagglutinin and neuraminidase genes are exchanged in an intermediate host. Clinical trials of candidate live attenuated influenza virus vaccines have shown the cold-adapted reassortants to be a promising alternative to the currently available inactivated virus preparations. Modern molecular techniques have allowed serious consideration of new approaches to the development of antiviral agents and vaccines as the functions of the viral genes and proteins are further elucidated. The development of techniques whereby the genes of influenza viruses can be specifically altered to investigate those functions will undoubtedly accelerate the pace at which our knowledge expands.

Animals↗