Viral Traits Research Articles

Remote sensing of temperature-dependent mosquito and viral traits predicts field surveillance-based disease risk.

Mosquito-borne diseases contribute substantially to the global burden of disease, and are strongly influenced by environmental conditions. Ongoing and rapid environmental change necessitates improved understanding of the response of mosquito-borne diseases to environmental factors like temperature, and novel approaches to mapping and monitoring risk. Recent development of trait-based mechanistic models has improved understanding of the temperature dependence of transmission, but model predictions remain challenging to validate in the field. Using West Nile virus (WNV) as a case study, we illustrate the use of a novel remote sensing-based approach to mapping temperature-dependent mosquito and viral traits at high spatial resolution and across the diurnal cycle. We validate the approach using mosquito and WNV surveillance data controlling for other key factors in the ecology of WNV, finding strong agreement between temperature-dependent traits and field-based metrics of risk. Moreover, we find that WNV infection rate in mosquitos exhibits a unimodal relationship with temperature, peaking at ~24.6-25.2°C, in the middle of the 95% credible interval of optimal temperature for transmission of WNV predicted by trait-based mechanistic models. This study represents one of the highest resolution validations of trait-based model predictions, and illustrates the utility of a novel remote sensing approach to predicting mosquito-borne disease risk.

Deep mutational scanning of SARS-CoV-2 Omicron BA.2.86 and epistatic emergence of the KP.3 variant.

Deep mutational scanning experiments aid in the surveillance and forecasting of viral evolution by providing prospective measurements of mutational effects on viral traits, but epistatic shifts in the impacts of mutations can hinder viral forecasting when measurements were made in outdated strain backgrounds. Here, we report measurements of the impact of all single amino acid mutations on ACE2-binding affinity and protein folding and expression in the SARS-CoV-2 Omicron BA.2.86 spike receptor-binding domain. As with other SARS-CoV-2 variants, we find a plastic and evolvable basis for receptor binding, with many mutations at the ACE2 interface maintaining or even improving ACE2-binding affinity. Despite its large genetic divergence, mutational effects in BA.2.86 have not diverged greatly from those measured in its Omicron BA.2 ancestor. However, we do identify strong positive epistasis among subsequent mutations that have accrued in BA.2.86 descendants. Specifically, the Q493E mutation that decreased ACE2-binding affinity in all previous SARS-CoV-2 backgrounds is reversed in sign to enhance human ACE2-binding affinity when coupled with L455S and F456L in the currently emerging KP.3 variant. Our results point to a modest degree of epistatic drift in mutational effects during recent SARS-CoV-2 evolution but highlight how these small epistatic shifts can have important consequences for the emergence of new SARS-CoV-2 variants.

Detection of HBV DNA by direct PCR protocol and Nested PCR protocol and comparing them in chronic patients and healthy carriers of Hepatitis B virus.

Hepatitis B virus is a major public health problem, and the outcome of infection depends on the effectiveness of the virus's interaction with the host, and in particular on the strength of the natural and conditioned response of humoral and cellular immunity. This study was conducted to assess the clinical status, genetic immunity and viral (viral) traits of Iraqi patients with chronic hepatitis B virus and healthy carriers of hepatitis B surface antigen, as well as to show the relationship between the immune status and the chronic condition of the disease. The study included (60) patients with chronic hepatitis B virus type (B) and (60) healthy hepatitis B surface antigen carriers who attended the Teaching Hospital for Gastrointestinal and Liver Diseases in Nasiriya City Al-Hussein Teaching Hospital, Thalassemia Center and the Central Blood Bank in Nasiriya Citysouthern of Iraq. for the period from the first period. From February 2022 until the end of February 2022, the average age of patients infected with chronic hepatitis B virus was 64.5 years, and the average age of healthy carriers of hepatitis B surface antigen was 35. 1 year, and the ratio of males to females was (12.2:) for chronic patients and (13.6:) for carriers of the disease. As for the deoxyribonucleic acid, it was (100%) in chronic patients and healthy carriers using the Nested type polymerase chain reaction, and at a rate of (30.0%) and (46.7%) in chronic patients and healthy carriers, respectively using the polymerase chain reaction technique. direct with a significant difference between the two interactions. The current results confirm that a nested PCR protocol to detect HBV DNA is a more sensitive way of detecting HBV in Iraq CHB patients and carriers. Recent advanced techniques such as nucleic acid assays, quantitative assays for viral load and RT-PCR for Iraqi viral hepatitis laboratories are recommended.

Accounting for cellular-level variation in lysis: implications for virus-host dynamics.

Viral impacts on microbial populations depend on interaction phenotypes-including viral traits spanning the adsorption rate, latent period, and burst size. The latent period is a key viral trait in lytic infections. Defined as the time from viral adsorption to viral progeny release, the latent period of bacteriophage is conventionally inferred via one-step growth curves in which the accumulation of free virus is measured over time in a population of infected cells. Developed more than 80 years ago, one-step growth curves do not account for cellular-level variability in the timing of lysis, potentially biasing inference of viral traits. Here, we use nonlinear dynamical models to understand how individual-level variation of the latent period impacts virus-host dynamics. Our modeling approach shows that inference of the latent period via one-step growth curves is systematically biased-generating estimates of shorter latent periods than the underlying population-level mean. The bias arises because variability in lysis timing at the cellular level leads to a fraction of early burst events, which are interpreted, artefactually, as an earlier mean time of viral release. We develop a computational framework to estimate latent period variability from joint measurements of host and free virus populations. Our computational framework recovers both the mean and variance of the latent period within simulated infections including realistic measurement noise. This work suggests that reframing the latent period as a distribution to account for variability in the population will improve the study of viral traits and their role in shaping microbial populations.IMPORTANCEQuantifying viral traits-including the adsorption rate, burst size, and latent period-is critical to characterize viral infection dynamics and develop predictive models of viral impacts across scales from cells to ecosystems. Here, we revisit the gold standard of viral trait estimation-the one-step growth curve-to assess the extent to which assumptions at the core of viral infection dynamics lead to ongoing and systematic biases in inferences of viral traits. We show that latent period estimates obtained via one-step growth curves systematically underestimate the mean latent period and, in turn, overestimate the rate of viral killing at population scales. By explicitly incorporating trait variability into a dynamical inference framework that leverages both virus and host time series, we provide a practical route to improve estimates of the mean and variance of viral traits across diverse virus-microbe systems.

Deep mutational scanning of SARS-CoV-2 Omicron BA.2.86 and epistatic emergence of the KP.3 variant.

Deep mutational scanning experiments aid in the surveillance and forecasting of viral evolution by providing prospective measurements of mutational effects on viral traits, but epistatic shifts in the impacts of mutations can hinder viral forecasting when measurements were made in outdated strain backgrounds. Here, we report measurements of the impact of all single amino acid mutations on ACE2-binding affinity and protein folding and expression in the SARS-CoV-2 Omicron BA.2.86 spike receptor-binding domain (RBD). As with other SARS-CoV-2 variants, we find a plastic and evolvable basis for receptor binding, with many mutations at the ACE2 interface maintaining or even improving ACE2-binding affinity. Despite its large genetic divergence, mutational effects in BA.2.86 have not diverged greatly from those measured in its Omicron BA.2 ancestor. However, we do identify strong positive epistasis among subsequent mutations that have accrued in BA.2.86 descendants. Specifically, the Q493E mutation that decreased ACE2-binding affinity in all previous SARS-CoV-2 backgrounds is reversed in sign to enhance human ACE2-binding affinity when coupled with L455S and F456L in the currently emerging KP.3 variant. Our results point to a modest degree of epistatic drift in mutational effects during recent SARS-CoV-2 evolution but highlight how these small epistatic shifts can have important consequences for the emergence of new SARS-CoV-2 variants.

Assembly of Glycopeptides in Living Cells Resembling Viral Infection for Cargo Delivery

AbstractSelf‐assembly in living cells represents one versatile strategy for drug delivery; however, it suffers from the limited precision and efficiency. Inspired by viral traits, we here report a cascade targeting‐hydrolysis‐transformation (THT) assembly of glycosylated peptides in living cells holistically resembling viral infection for efficient cargo delivery and combined tumor therapy. We design a glycosylated peptide via incorporating a β‐galactose‐serine residue into bola‐amphiphilic sequences. Co‐assembling of the glycosylated peptide with two counterparts containing irinotecan (IRI) or ligand TSFAEYWNLLSP (PMI) results in formation of the glycosylated co‐assemblies SgVEIP, which target cancer cells via β‐galactose‐galectin‐1 association and undergo galactosidase‐induced morphological transformation. While GSH‐reduction causes release of IRI from the co‐assemblies, the PMI moieties release p53 and facilitate cell death via binding with protein MDM2. Cellular experiments show membrane targeting, endo‐/lysosome‐mediated internalization and in situ formation of nanofibers in cytoplasm by SgVEIP. This cascade THT process enables efficient delivery of IRI and PMI into cancer cells secreting Gal‐1 and overexpressing β‐galactosidase. In vivo studies illustrate enhanced tumor accumulation and retention of the glycosylated co‐assemblies, thereby suppressing tumor growth. Our findings demonstrate an in situ assembly strategy mimicking viral infection, thus providing a new route for drug delivery and cancer therapy in the future.

Assembly of Glycopeptides in Living Cells Resembling Viral Infection for Cargo Delivery.

Self-assembly in living cells represents one versatile strategy for drug delivery; however, it suffers from the limited precision and efficiency. Inspired by viral traits, we here report a cascade targeting-hydrolysis-transformation (THT) assembly of glycosylated peptides in living cells holistically resembling viral infection for efficient cargo delivery and combined tumor therapy. We design a glycosylated peptide via incorporating a β-galactose-serine residue into bola-amphiphilic sequences. Co-assembling of the glycosylated peptide with two counterparts containing irinotecan (IRI) or ligand TSFAEYWNLLSP (PMI) results in formation of the glycosylated co-assemblies SgVEIP, which target cancer cells via β-galactose-galectin-1 association and undergo galactosidase-induced morphological transformation. While GSH-reduction causes release of IRI from the co-assemblies, the PMI moieties release p53 and facilitate cell death via binding with protein MDM2. Cellular experiments show membrane targeting, endo-/lysosome-mediated internalization and in situ formation of nanofibers in cytoplasm by SgVEIP. This cascade THT process enables efficient delivery of IRI and PMI into cancer cells secreting Gal-1 and overexpressing β-galactosidase. In vivo studies illustrate enhanced tumor accumulation and retention of the glycosylated co-assemblies, thereby suppressing tumor growth. Our findings demonstrate an in situ assembly strategy mimicking viral infection, thus providing a new route for drug delivery and cancer therapy in the future.

Transcriptomic alterations in host parasitoid wasps resulting in extended lifespan due to PpNSRV-1 infection

The parasitoid wasp Pteromalus puparum, a pivotal agent in agricultural ecosystem balance, experiences significant alterations in lifespan due to infection by the negative-sense single-stranded RNA virus PpNSRV-1. This study utilized RNA sequencing (RNA-seq) to investigate the genetic mechanism(s) driving lifespan extension in response to this virus. Lifespan analysis, combined with RNA-seq of nearly isogenic lines of infected and uninfected wasps, yields a comprehensive temporal expression profile aligned with the P. puparum genome. Despite a modest overall impact of PpNSRV-1 on gene expression, notable effects were observed on specific gene families, such as the SPOP genes and the cytochrome P450 family. Through Weighted Gene Co-expression Network Analysis (WGCNA), we identified connections between the green and greenyellow modules to viral infection traits, with further functional analyses highlighting the pivotal roles of the Hedgehog, autophagy, AMPK, mTOR, p53, and PI3K-Akt signaling pathways. RNA interference experiment targeting the SPOP gene PPU06594-RA confirmed its role in lifespan modulation, underscoring the importance of Hedgehog pathway in the host’s adaptive response. These insights not only elucidate the complex genetic landscape of host-virus interactions but also open avenues for innovative biological pest control strategies.

Detection of Hbv Dna By Direct Pcr Protocol And Nested Pcr Protocol And Comparing Them. In Chronic Patients and Healthy Carriers of Hepatitis B Virus.

Hepatitis B virus is a major public health problem, and the outcome of infection depends on the effectiveness of the virus's interaction with the host, and in particular on the strength of the natural and conditioned response of humoral and cellular immunity. This study was conducted to assess the clinical status, genetic immunity and viral (viral) traits of Iraqi patients with chronic hepatitis B virus and healthy carriers of hepatitis B surface antigen, as well as to show the relationship between the immune status and the chronic condition of the disease. The study included (60) patients with chronic hepatitis B virus type (B) and (60) healthy hepatitis B surface antigen carriers who attended the Teaching Hospital for Gastrointestinal and Liver Diseases in Nasiriya City Al-Hussein Teaching Hospital, Thalassemia Center and the Central Blood Bank in Nasiriya Citysouthern of Iraq. for the period from the first period. From February 2022 until the end of February 2022, the average age of patients infected with chronic hepatitis B virus was 64.5 years, and the average age of healthy carriers of hepatitis B surface antigen was 35. 1 year, and the ratio of males to females was (12.2:) for chronic patients and (13.6:) for carriers of the disease. As for the deoxyribonucleic acid, it was (100%) in chronic patients and healthy carriers using the Nested type polymerase chain reaction, and at a rate of (30.0%) and (46.7%) in chronic patients and healthy carriers, respectively using the polymerase chain reaction technique. direct with a significant difference between the two interactions. The current results confirm that a nested PCR protocol to detect HBV DNA is a more sensitive way of detecting HBV in Iraq CHB patients and carriers. Recent advanced techniques such as nucleic acid assays, quantitative assays for viral load and RT-PCR for Iraqi viral hepatitis laboratories are recommended.

Disentangling top-down drivers of mortality underlying diel population dynamics of Prochlorococcus in the North Pacific Subtropical Gyre

Photosynthesis fuels primary production at the base of marine food webs. Yet, in many surface ocean ecosystems, diel-driven primary production is tightly coupled to daily loss. This tight coupling raises the question: which top-down drivers predominate in maintaining persistently stable picocyanobacterial populations over longer time scales? Motivated by high-frequency surface water measurements taken in the North Pacific Subtropical Gyre (NPSG), we developed multitrophic models to investigate bottom-up and top-down mechanisms underlying the balanced control of Prochlorococcus populations. We find that incorporating photosynthetic growth with viral- and predator-induced mortality is sufficient to recapitulate daily oscillations of Prochlorococcus abundances with baseline community abundances. In doing so, we infer that grazers in this environment function as the predominant top-down factor despite high standing viral particle densities. The model-data fits also reveal the ecological relevance of light-dependent viral traits and non-canonical factors to cellular loss. Finally, we leverage sensitivity analyses to demonstrate how variation in life history traits across distinct oceanic contexts, including variation in viral adsorption and grazer clearance rates, can transform the quantitative and even qualitative importance of top-down controls in shaping Prochlorococcus population dynamics.

Study on Italian Onion Cultivars/Ecotypes towards Onion Yellow Dwarf Virus (OYDV) Infection

The onion yellow dwarf virus (OYDV) represents a limiting biotic stress in onion (Allium cepa L.); little information is available regarding resistant varieties. In Italy, onion production is limited but represented by a wide diversity of ecotypes. A two-year trial was carried out to test the OYDV-susceptibility/tolerance of different Italian onion cultivars by rating symptom severity and plant growth parameters and assessing post-harvest secondary infections. The cultivar and ecotypes included in the study were characterized by simple sequence repeats (SSR) analysis, and the expression analysis of two genes (Eukaryotic translation initiation factors, EIFs) involved in potyvirus replication was also performed. Two susceptible and one tolerant cultivar were identified based on symptom expression and virus impact on plants. Although differences in growth parameters were limited to the first-year trial, the infection was correlated to a higher incidence of secondary infections in post-harvest, with altered water balance in infected bulbs. This correlation was also demonstrated during the long-term storage of bulbs. SSR analysis identified different clusters and only one gene isoform (EIF4eiso1) showed different expression levels in the OYDV/onion pathosystem. In conclusion, this study defines the genetic profile of Italian onion cultivars and provides evidence on susceptibility/tolerance features which will be useful in the future for the identification of viral resistance traits in onion.

The structure and assembly mechanisms of T4-like cyanophages community in the South China Sea.

Marine ecosystems contain an immense diversity of phages, many of which infect cyanobacteria (cyanophage) that are largely responsible for primary productivity. To characterize the genetic diversity and biogeographic distribution of the marine T4-like cyanophage community in the northern South China Sea, the T4-like cyanophage portal protein gene (g20) was amplified. Phylogenetic analysis revealed that marine T4-like cyanophages were highly diverse, with g20 operational taxonomic units being affiliated with five defined clades (Clusters I-V). Cluster II had a wide geographic distribution, Cluster IV was the most abundant in the open sea, and Cluster I was dominant in coastal shelf environments. Our results showed T4-like cyanophages (based on g20) community was generally shaped via heterogeneous selection. Highly variable environmental factors (such as salinity and temperature) can heterogeneously select different cyanophage communities. Nevertheless, the dominant drivers of the T4-like cyanophage community based on the g20 and g23 (T4-like phage major capsid protein gene) were different, probably due to different coverages by the primer sets. Furthermore, the community assembly processes of T4-like cyanophages were affected by host traits (abundance and distribution), viral traits (latent period, burst size, and host range), and environmental properties (temperature and salinity).IMPORTANCECyanophages are abundant and ubiquitous in the oceans, altering population structures and evolution of cyanobacteria, which account for a large portion of global carbon fixation, through host mortality, horizontal gene transfer, and the modulation of host metabolism. However, little is known about the biogeography and ecological drivers that shape the cyanophage community. Here, we use g20 and g23 genes to examine the biogeographic patterns and the assembly mechanisms of T4-like cyanophage community in the northern part of the South China Sea. The different coverages of primer sets might lead to the different dominant drivers of T4-like cyanophage community based on g20 and g23 genes. Our results showed that characteristics of viral traits (latent period, burst size, and host range) and host traits (abundance and distribution) were found to either limit or enhance the biogeographic distribution of T4-like cyanophages. Overall, both virus and host properties are critical to consider when determining rules of community assembly for viruses.

Avian influenza virus cross-infections as test case for pandemic preparedness: From epidemiological hazard models to sequence-based early viral warning systems.

Pandemic preparedness starts with an early warning system of viruses with a pandemic potential. Based on information collected in a multitude of surveys, hazard models were developed identifying influenza viruses presenting a pandemic threat. Scores are attributed for 10 viral traits by expert panels which identified avian influenza viruses (AIV) belonging to subtypes H7N9 and H5N1 as representing the greatest pandemic risk. In 2013, more than 100 human cases infected with AIV H7N9 were observed in China. Case fatality rate (CFR) was high (27%), but the human-to-human transmission rate was low and by serological evidence H7N9 did not spread widely. Nevertheless, until 2019 more than 1500 H7N9 patients were identified characterized by a high CFR of 39%. Serology demonstrated that mild infections with H7N9 were widespread. In 2003, more than 400 people experienced AIV H7N7 cross-infection causing mainly conjunctivitis during a large poultry epidemic in The Netherlands. Between 1996 and 2019, a total of 881 human infections with avian H5N1 viruses were documented showing a CFR of 52%. Outbreaks were centred on South East Asia and showed close associations with epizootics in poultry. Mutations predisposing to human cross-infections were identified in the haemagglutinin (HA) and the RNA polymerase subunit PB2 of human H7N9 isolates. Human H5N1 isolates showed mutations in the receptor binding domain of HA and transmission in mammals could be obtained by as few as four additional aa changes introduced experimentally. Researchers have defined viral point mutations in HA, PB2 and the nucleoprotein NP that allowed AIV to cross the species barrier to mammals with respect to receptor recognition, RNA replication and escape from innate immunity respectively. Based on this insight a sequence-based early warning system for AIV preadapted to human transmission could be envisioned. Mink farms and live poultry markets are prime targets for such sequencing efforts.

Global diversity and biogeography of DNA viral communities in activated sludge systems

BackgroundActivated sludge (AS) systems in wastewater treatment plants (WWTPs) harbor enormous viruses that regulate microbial metabolism and nutrient cycling, significantly influencing the stability of AS systems. However, our knowledge about the diversity of viral taxonomic groups and functional traits in global AS systems is still limited. To address this gap, we investigated the global diversity and biogeography of DNA viral communities in AS systems using 85,114 viral operational taxonomic units (vOTUs) recovered from 144 AS samples collected across 54 WWTPs from 13 different countries.ResultsAS viral communities and their functional traits exhibited distance-decay relationship (DDR) at the global scale and latitudinal diversity gradient (LDG) from equator to mid-latitude. Furthermore, it was observed that AS viral community and functional gene structures were largely driven by the geographic factors and wastewater types, of which the geographic factors were more important. Carrying and disseminating auxiliary metabolic genes (AMGs) associated with the degradation of polysaccharides, sulfate reduction, denitrification, and organic phosphoester hydrolysis, as well as the lysis of crucial functional microbes that govern biogeochemical cycles were two major ways by which viruses could regulate AS functions. It was worth noting that our study revealed a high abundance of antibiotic resistance genes (ARGs) in viral genomes, suggesting that viruses were key reservoirs of ARGs in AS systems.ConclusionsOur results demonstrated the highly diverse taxonomic groups and functional traits of viruses in AS systems. Viral lysis of host microbes and virus-mediated HGT can regulate the biogeochemical and nutrient cycles, thus affecting the performance of AS systems. These findings provide important insights into the viral diversity, function, and ecology in AS systems on a global scale.-K8pwvbs3fYC6bGWQ-q_MyVideo

A new member of the Nudiviridae from the Florida stone crab (Menippe mercenaria)

Menippe mercenaria, the Florida stone crab, supports an unconventional fishery across the southern USA and Caribbean that involves claw-removal and the return of de-clawed animals to the sea. We provide pathological, ultrastructural, and genomic detail for a novel hepatopancreatic, nucleus-specific virus - Menippe mercenaria nudivirus (MmNV) - isolated from M. mercenaria, captured during fisheries-independent monitoring.The virus has a genome of 99,336 bp and encodes 84 predicted protein coding genes and shows greatest similarity to Aratus pisonii nudivirus (ApNV) (<60% protein similarity and 31 shared genes of greatest similarity), collected from the Florida Keys, USA. MmNV is a member of the Gammanudivirus genus (Naldaviricetes: Lefavirales: Nudiviridae). Comparisons of virus genome size, preferred host environment, and gene number revealed no clear associations between the viral traits and phylogenetic position. Evolution of the virus alongside the diversification of host taxa, with the potential for host-switching, remain more likely evolutionary pathways.

Reservoir host immunology and life history shape virulence evolution in zoonotic viruses.

The management of future pandemic risk requires a better understanding of the mechanisms that determine the virulence of emerging zoonotic viruses. Meta-analyses suggest that the virulence of emerging zoonoses is correlated with but not completely predictable from reservoir host phylogeny, indicating that specific characteristics of reservoir host immunology and life history may drive the evolution of viral traits responsible for cross-species virulence. In particular, bats host viruses that cause higher case fatality rates upon spillover to humans than those derived from any other mammal, a phenomenon that cannot be explained by phylogenetic distance alone. In order to disentangle the fundamental drivers of these patterns, we develop a nested modeling framework that highlights mechanisms that underpin the evolution of viral traits in reservoir hosts that cause virulence following cross-species emergence. We apply this framework to generate virulence predictions for viral zoonoses derived from diverse mammalian reservoirs, recapturing trends in virus-induced human mortality rates reported in the literature. Notably, our work offers a mechanistic hypothesis to explain the extreme virulence of bat-borne zoonoses and, more generally, demonstrates how key differences in reservoir host longevity, viral tolerance, and constitutive immunity impact the evolution of viral traits that cause virulence following spillover to humans. Our theoretical framework offers a series of testable questions and predictions designed to stimulate future work comparing cross-species virulence evolution in zoonotic viruses derived from diverse mammalian hosts.

SARS-CoV-2 variants, its recombinants and epigenomic exploitation of host defenses

Since 2003, we have seen the emergence of novel viruses, such as SARS-CoV-1, MERS, ZIKA, swine flu virus H1N1, Marburg, Monkeypox, Ebola, and SARS-CoV-2, but none of them gained pandemic proportions similar to SARS-CoV-2. This could be attributed to unique viral traits, allowing its rapid global dissemination following its emergence in October 2019 in Wuhan, China, which appears to be primarily driven by the emergence of highly transmissible and virulent variants that also associate, in some cases, with severe disease and considerable mortality caused by fatal pneumonia, acute respiratory distress syndrome (ARDS) in infected individuals.Mechanistically, several factors are involved in viral pathogenesis, and epigenetic alterations take the front seat in host-virus interactions. The molecular basis of all viral infections, including SARS-CoV-2, tightly hinges on the transitory silencing of the host gene machinery via epigenetic modulation. SARS-CoV-2 also hijacks and subdues the host gene machinery, leading to epigenetic modulation of the critical host elements responsible for antiviral immunity. Epigenomics is a powerful, unexplored avenue that can provide a profound understanding of virus-host interactions and lead to the development of epigenome-based therapies and vaccines to counter viruses. This review discusses current developments in SARS-CoV-2 variation and its role in epigenetic modulation in infected hosts. This review provides an overview, especially in the context of emerging viral strains, their recombinants, and their possible roles in the epigenetic exploitation of host defense and viral pathogenesis. It provides insights into host-virus interactions at the molecular, genomic, and immunological levels and sheds light on the future of epigenomics-based therapies for SARS-CoV-2 infection.

Pandemic potential of poxviruses: From an ancient killer causing smallpox to the surge of monkeypox.

Smallpox caused by the variola virus (VARV) was one of the greatest infectious killers of mankind. Historical records trace back smallpox for at least a millennium while phylogenetic analysis dated the ancestor of VARV circulating in the 20th century into the 19th century. The discrepancy was solved by the detection of distinct VARV sequences first in 17th-century mummies and then in human skeletons dated to the 7th century. The historical records noted marked variability in VARV virulence which scientists tentatively associated with gene losses occurring when broad-host poxviruses narrow their host range to a single host. VARV split from camel and gerbil poxviruses and had no animal reservoir, a prerequisite for its eradication led by WHO. The search for residual pockets of VARV led to the discovery of the monkeypox virus (MPXV); followed by the detection of endemic smallpox-like monkeypox (mpox) disease in Africa. Mpox is caused by less virulent clade 2 MPXV in West Africa and more virulent clade 1 MPXV in Central Africa. Exported clade 2 mpox cases associated with the pet animal trade were observed in 2003 in the USA. In 2022 a world-wide mpox epidemic infecting more than 80,000 people was noted, peaking in August 2022 although waning rapidly. The cases displayed particular epidemiological characteristics affecting nearly exclusively young men having sex with men (MSM). In contrast, mpox in Africa mostly affects children by non-sexual transmission routes possibly from uncharacterized animal reservoirs. While African children show a classical smallpox picture, MSM mpox cases show few mostly anogenital lesions, low-hospitalization rates and 140 fatal cases worldwide. MPXV strains from North America and Europe are closely related, derived from clade 2 African MPXV. Distinct transmission mechanisms are more likely causes for the epidemiological and clinical differences between endemic African cases and the 2022 epidemic cases than viral traits.

Assessment and sero-diagnosis for coronaviruses with risk of human spillover

ABSTRACT Zoonotic coronaviruses (CoVs) caused major human outbreaks in the last two decades. One of the biggest challenges during future CoV disease is ensuring rapid detection and diagnosis at the early phase of a zoonotic event, and active surveillance to the zoonotic high-risk CoVs appears the best way at the present time to provide early warnings. However, there is neither an evaluation of spillover potential nor diagnosis tools for the majority of CoVs. Here, we analyzed the viral traits, including population, genetic diversity, receptor and host species for all 40 alpha- and beta-CoV species, where the human-infecting CoVs are from. Our analysis proposed 20 high-risk CoV species, including 6 of which jumped to human, 3 with evidence of spillover but not to human and 11 without evidence of spillover yet, which prediction were further supported by an analysis of the history of CoV zoonosis. We also found three major zoonotic sources: multiple bat-origin CoV species, the rodent-origin sub-genus Embecovirus and the CoV species AlphaCoV1. Moreover, the Rhinolophidae and Hipposideridae bats harbour a significantly higher proportion of human-threatening CoV species, whereas camel, civet, swine and pangolin could be important intermediate hosts during CoV zoonotic transmission. Finally, we established quick and sensitive serologic tools for a list of proposed high-risk CoVs and validated the methods in serum cross-reaction assays using hyper-immune rabbit sera or clinical samples. By comprehensive risk assessment of the potential human-infecting CoVs, our work provides a theoretical or practical basis for future CoV disease preparedness.

유전 알고리즘을 적용한 바이러스의 진화와 확산 시뮬레이션 제작

In this study, Genetic Algorithm was introduced to simulate virus mutation and to understand the changes in viral traits and human immunity. In the simulation, humans move randomly and social distancing measures are implemented when the number of infected humans exceeds 5%. The virus is defined by two traits: the infection rate between humans and the virus attack, represented by strings and floating-point genes, respectively. The progression of the disease is calculated through the “life system” based on the competition between the virus attack and the human recovery rate. The viruses were classified into subspecies based on genetic similarity. Through analysis of the changes in traits per species, it was concluded that an increase in infection rate and a decrease in virus attack within the body were favorable variations for the survival of the virus. Simulation results were compared with the daily new confirmed COVID-19 cases in Sweden, demonstrating accuracy of the simulation. This simulation is more realistic and adaptable in terms of the implementation of mutations and immunity compared to existing spread models. It is expected that by analyzing the effectiveness of quarantine policies, the damage caused by infectious diseases could be reduced drastically.