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        <title>Frontiers in Virology | Viral Diversification and Evolution section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/virology/sections/viral-diversification-and-evolution</link>
        <description>RSS Feed for Viral Diversification and Evolution section in the Frontiers in Virology journal | New and Recent Articles</description>
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        <pubDate>2026-05-14T20:11:10.350+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2025.1696495</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2025.1696495</link>
        <title><![CDATA[Editorial: Epidemiology and control of blood-borne viruses in low- and middle-income countries: genomic insights and public health strategies]]></title>
        <pubdate>2025-10-13T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Nidia S. Trovao</author><author>Sana Tamim</author><author>Marceline Djuidje Ngounoue</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2025.1619249</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2025.1619249</link>
        <title><![CDATA[Current trends in the epidemiology and management of viral co-infections and comorbidities in Africa: a systematic review]]></title>
        <pubdate>2025-08-01T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Axel Cyriaque Ambassa</author><author>Fabrice Chethkwo</author><author>Elise Guiedem</author><author>Brenda Grace Lele</author><author>Ironne Valdese Ayemfouo Fofou</author><author>Marceline Djuidje Ngounoue</author>
        <description><![CDATA[BackgroundViral infections, particularly hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis Delta virus (HDV), and human immunodeficiency virus (HIV), pose significant public health challenges worldwide, especially in low- and middle-income countries (LMICs) in Africa. The diagnosis and management of these diseases become increasingly complicated when viral co-infections are present. This review aims to explore current trends in the epidemiology and management of viral co-infections and comorbidities in LMICs.MethodsA systematic review was conducted following the PRISMA-ScR (Preferred Reporting Items for Systematic and Meta-Analyses extension for Scoping Reviews) guidelines. A thorough literature search was performed across two databases: PubMed and Google Scholar. A total of 390 records were identified from PubMed, and approximately 17,000 from Google Scholar for studies published between 2015 and 2025. After removing duplicates and applying eligibility criteria, 50 articles from PubMed were screened based on their titles, abstracts, and full texts. Of these, 15 studies that met the inclusion criteria were selected for data extraction and synthesis, using a data extraction form to organize the relevant information.ResultsOut of the 50 screened studies, 15 met the inclusion criteria and were included in the final analysis. These studies primarily focused on co-infections of HIV with HBV and HCV. The prevalence rates of HBV among individuals living with HIV varied from 1.1% to 9.1% in cross-sectional studies, with notable populations including pre-ART patients and pregnant women. One study reported a particularly high rate of HCV co-infection at 66.6% among intravenous drug users. However, no eligible studies were available for HBV-HDV co-infection or treatment-specific outcomes.ConclusionThis review highlights the significant burden and variability of HIV co-infections in Africa, particularly the co-infection of HIV with HBV. The findings emphasize the necessity for integrated screening and management strategies, as well as the need for further research to optimize interventions and improve health outcomes for individuals with co-infections.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1527580</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1527580</link>
        <title><![CDATA[Editorial: Impact of the SARS-CoV-2 pandemic on the evolution and epidemiology of other viruses]]></title>
        <pubdate>2024-12-19T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Alfonso J. Rodríguez-Morales</author><author>Jorge X. Velasco-Hernández</author><author>Andreu Comas-Garcia</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1399993</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1399993</link>
        <title><![CDATA[An overview of SARS-CoV-2 viral proteins with relevance to improved diagnostic and therapeutic platforms]]></title>
        <pubdate>2024-10-03T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Christopher Chung</author><author>Pratiba Irudayaraj</author><author>Emran Lallow</author><author>Ziyang Xu</author><author>Young K. Park</author><author>Sagar B. Kudchodkar</author><author>Luis J. Montaner</author><author>Alagarsamy Srinivasan</author><author>Kar Muthumani</author>
        <description><![CDATA[In the past 25 years, the world has witnessed outbreaks of illnesses in humans from three different coronaviruses. Both the SARS-CoV outbreak of 2003 and the MERS-CoV outbreak of 2013 resulted in overall low fatalities in part due to inefficient human-to-human spread of each virus. In contrast, SARS-CoV-2, which emerged in 2019, was highly efficient at human-to-human spread and caused a global pandemic resulting in millions of casualties. Zoonotic transmission of viruses, including the three coronaviruses, poses an ongoing threat that cannot be ignored. In this review, we have focused on the diagnostics and therapeutics fronts using SARS-CoV-2 as a model. Specifically, we have selected proteins associated with the virus particles as targets and discussed various platform technologies. These insights hold the potential to inform the development of more effective therapeutics and vaccines not only for SARS-CoV-2 but also for future viral pandemics, thus contributing to global health on a broader scale.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1465702</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1465702</link>
        <title><![CDATA[Editorial: Characterization of HIV-1 variants: implications for HIV-1 prevention, treatment and cure]]></title>
        <pubdate>2024-08-16T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Jaclyn K. Mann</author><author>Marcel Tongo</author><author>Takamasa Ueno</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1433931</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1433931</link>
        <title><![CDATA[Phylogenetic-based methods for fine-scale classification of PRRSV-2 ORF5 sequences: a comparison of their robustness and reproducibility]]></title>
        <pubdate>2024-08-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kimberly VanderWaal</author><author>Nakarin Pamornchainavakul</author><author>Mariana Kikuti</author><author>Daniel C. L. Linhares</author><author>Giovani Trevisan</author><author>Jianqiang Zhang</author><author>Tavis K. Anderson</author><author>Michael Zeller</author><author>Stephanie Rossow</author><author>Derald J. Holtkamp</author><author>Dennis N. Makau</author><author>Cesar A. Corzo</author><author>Igor A. D. Paploski</author>
        <description><![CDATA[Disease management and epidemiological investigations of porcine reproductive and respiratory syndrome virus-type 2 (PRRSV-2) often rely on grouping together highly related sequences. In the USA, the last five years have seen a major shift within the swine industry when classifying PRRSV-2, beginning to move away from RFLP (restriction fragment length polymorphisms)-typing and adopting the use of phylogenetic lineage-based classification. However, lineages and sub-lineages are large and genetically diverse, making them insufficient for identifying new and emerging variants. Thus, within the lineage system, a dynamic fine-scale classification scheme is needed to provide better resolution on the relatedness of PRRSV-2 viruses to inform disease management and monitoring efforts and facilitate research and communication surrounding circulating PRRSV viruses. Here, we compare fine-scale systems for classifying PRRSV-2 variants (i.e., genetic clusters of closely related ORF5 sequences at finer scales than sub-lineage) using a database of 28,730 sequences from 2010 to 2021, representing >55% of the U.S. pig population. In total, we compared 140 approaches that differed in their tree-building method, criteria, and thresholds for defining variants within phylogenetic trees. Three approaches resulted in variant classifications that were reproducible and robust even when the input data or input phylogenies were changed. For these approaches, the average genetic distance among sequences belonging to the same variant was 2.1–2.5%, and the genetic divergence between variants was 2.5–2.7%. Machine learning classification algorithms were trained to assign new sequences to an existing variant with >95% accuracy, which shows that newly generated sequences can be assigned to a variant without repeating the phylogenetic and clustering analyses. Finally, we identified 73 sequence-clusters (dated <1 year apart with close phylogenetic relatedness) associated with circulation events on single farms. The percent of farm sequence-clusters with an ID change was 6.5–8.7% for our approaches. In contrast, ~43% of farm sequence-clusters had variation in their RFLP-type, further demonstrating how our proposed fine-scale classification system addresses shortcomings of RFLP-typing. Through identifying robust and reproducible classification approaches for PRRSV-2, this work lays the foundation for a fine-scale system that would more reliably group related field viruses and provide better resolution for decision-making surrounding disease management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1393475</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1393475</link>
        <title><![CDATA[HIV latency potential may be influenced by intra-subtype genetic differences in the viral long-terminal repeat]]></title>
        <pubdate>2024-06-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Deelan Sudhir Doolabh</author><author>Philippe Selhorst</author><author>Carolyn Williamson</author><author>Denis Chopera</author><author>Melissa-Rose Abrahams</author>
        <description><![CDATA[IntroductionElucidation of mechanisms that drive HIV latency is essential to identifying cure strategies. While host mechanisms associated with viral persistence on antiretroviral therapy (ART) have been well studied, less is known about the viral properties that influence latency. The viral promoter element, the 5’ long terminal repeat (LTR), has been shown to affect the number of latently infected cells shortly after infection. Here we investigated the role of subtype C LTR genotypic variation on the establishment of latency in a dual reporter HIV-1 infection model.MethodsThe LTR U3 and R regions from 11 women with acute/early subtype C HIV infection were cloned into the dual reporter pRGH plasmid. Latency potential was calculated based on the expression of fluorescent reporter genes in Jurkat E6–1 cells measured by flow cytometry as the proportion of latent (mCherry +ve cells)/proportion of active (eGFP +ve mCherry +ve cells) infection. Reversal of latency was performed using PMA/Ionomycin stimulation 24 hours before fixing of cells. LTR transcriptional capacity, in the presence and absence of a heterologous subtype C Tat, was measured for the same LTRs cloned into a pGL4.10 luciferase expression vector following transfection of HEK293T cells.ResultsThe majority of proviruses were latent at day 8 post-infection, yet the proportion of latently infected cells varied significantly across participants. We observed a median latent:active infection ratio of 1.79 (range 0.86–2.83) across LTRs with the hierarchy of latency potential remaining consistent across repeat experiments. The median latent:active infection ratio decreased by a median of 3-fold following PMA/Ionomycin stimulation to 0.55 (range 0.46–0.78) indicating that a proportion of latently infected cells could produce viral proteins upon activation. Latency potential did not correlate with LTR transcriptional capacity.ConclusionsWe found intra-subtype level differences in the latency potential of LTRs from South African women independent of their transcriptional capacity, suggesting that HIV-1 LTRs have intrinsic properties that influence the proportion of latently infected cells shortly after infection. The inability to reactivate viral expression in all latently infected cells supports the complex nature of mechanisms driving latency and the need for continued advancements in methods used to study these mechanisms.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1379217</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1379217</link>
        <title><![CDATA[No detectable differences in Nef-mediated downregulation of HLA-I and CD4 molecules among HIV-1 group M lineages circulating in Cameroon, where the pandemic originated]]></title>
        <pubdate>2024-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nelson Sonela</author><author>Jaclyn Mann</author><author>Celestin Godwe</author><author>Oumarou H. Goni</author><author>Mérime Tchakoute</author><author>Nathalie Nkoue</author><author>Tulio de Oliveira</author><author>Mark A. Brockman</author><author>Zabrina L. Brumme</author><author>Thumbi Ndung’u</author><author>Marcel Tongo</author>
        <description><![CDATA[HIV-1 group M (HIV-1M) lineages downregulate HLA-I and CD4 expression via their Nef proteins. We hypothesized that these Nef functions may be partially responsible for the differences in prevalence of viruses from different lineages that co-circulate within an epidemic. Here, we characterized these two Nef activities in HIV-1M isolates from Cameroon, where multiple variants have been circulating since the pandemic’s origin. Single HIV-1 Nef clones from 234 HIV-1-ART naïve individuals living in remote villages and two cosmopolitan cities of Cameroon, sampled between 2000 and 2013, were isolated from plasma HIV RNA and analyzed for their capacity to downregulate HLA-I and CD4 molecules. We found that, despite a large degree of within- and inter- lineage variation, the ability of Nef to downregulate HLA-I was similar across these different viruses. Moreover, Nef-mediated CD4 downregulation activity was also well conserved across the different lineages found in Cameroon. In addition, we observed a trend towards higher HLA-I downregulation activity of viruses circulating in the cosmopolitan cities versus the remote villages, whereas the CD4 downregulation activities were similar across the two settings. Furthermore, we noted a significant decline of HLA-I downregulation activity from 2000 to 2013, providing additional evidence supporting the attenuation of the global HIV-1M population over time. Finally, we identified 18 amino acids associated with differential HLA-I downregulation and 13 amino acids associated with differential CD4 downregulation within the dominant CRF02_AG lineage. Our lack of observation of HIV lineage-related differences in Nef-mediated HLA-I and CD4 downregulation function suggests that these activities do not substantively influence the prevalence of different HIV-1M lineages in Cameroon.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2024.1363092</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2024.1363092</link>
        <title><![CDATA[Evolutionary engineering and characterization of Sendai virus mutants capable of persistent infection and autonomous production]]></title>
        <pubdate>2024-04-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Moe Iwata</author><author>Ryoko Kawabata</author><author>Nao Morimoto</author><author>Ryosuke F. Takeuchi</author><author>Takemasa Sakaguchi</author><author>Takashi Irie</author><author>Fumitaka Osakada</author>
        <description><![CDATA[Persistent virus infection involves modifying the host immune response and maintaining viral infection. Acute infection with Mononegavirales, such as Sendai viruses (SeVs), can give rise to viruses capable of persistent infection. SeVs establish persistent infection through generating copyback-type defective interfering (cbDI) genomes or acquiring temperature-sensitive mutations. Herein, we identify novel mutations associated with persistent infection and recombinant SeV mutants capable of persistent infection and autonomous production at physiological body temperature, independent of cbDI genomes or temperature-sensitive mutations. Diverse SeV populations were generated by passing the cDNA-recovered SeV Z strain 19 times through embryonated chicken eggs and subsequently infecting LLC-MK2 cells with the SeV populations to finally obtain SeV mutants capable of persistent infection and autonomous production in several types of cultured cells. Sequence analysis identified 4 or 5 mutations in the genome of the persistently infectious SeVs, distinguishing them from other existing strains with persistent infection. Recombinant SeVs carrying 4 or 5 mutations in the Z strain genome (designated SeV-Zpi or SeV-Zpi2, respectively) exhibited persistent infection and autonomous production in LLC-MK2, BHK-21, and Neuro2a cells at 37°C. SeV-Zpi and SeV-Zpi2 consistently produced viral particles even after long-term passages without cbDI particles or temperature-sensitive phenotypes. These results highlight the ability of acute infections of SeVs to spontaneously acquire mutations during replication, thereby endowing persistent infection and autonomous production at body temperature. The vectorization of SeV-Zpi and SeV-Zpi2 will contribute to both basic research and medical applications.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1291996</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1291996</link>
        <title><![CDATA[Evolution driven by a varying host environment selects for distinct HIV-1 entry phenotypes and other informative variants]]></title>
        <pubdate>2023-11-16T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Shuntai Zhou</author><author>Nathan Long</author><author>Ronald Swanstrom</author>
        <description><![CDATA[HIV-1 generates remarkable intra- and inter-host viral diversity during infection. In the response to the dynamic selective pressures of the host’s environment, HIV-1 evolves distinct phenotypes—biological features that provide fitness advantages. The transmitted form of HIV-1 has been shown to require a high density of CD4 on the target cell surface (as found on CD4+ T cells) and typically uses C–C chemokine receptor type 5 (CCR5) as a coreceptor during entry. This phenotype is referred to as R5T cell-tropic (or R5 T-tropic); however, HIV-1 can switch to a secondary coreceptor, C–X–C chemokine receptor type 4 (CXCR4), resulting in a X4T cell-tropic phenotype. Macrophage-tropic (or M-tropic) HIV-1 can evolve to efficiently enter cells expressing low densities of CD4 on their surface (such as macrophages/microglia). So far only CCR5-using M-tropic viruses have been found. M-tropic HIV-1 is most frequently found within the central nervous system (CNS), and infection of the CNS has been associated with neurologic impairment. It has been shown that interferon-resistant phenotypes have a selective advantage during transmission, but the underlying mechanism of this is still unclear. During untreated infection, HIV-1 evolves under selective pressure from both the humoral/antibody response and CD8+ T-cell killing. Sufficiently potent antiviral therapy can suppress viral replication, but if the antiviral drugs are not powerful enough to stop replication, then the replicating virus will evolve drug resistance. HIV-1 phenotypes are highly relevant to treatment efforts, clinical outcomes, vaccine studies, and cure strategies. Therefore, it is critical to understand the dynamics of the host environment that drive these phenotypes and how they affect HIV-1 pathogenesis. This review will provide a comprehensive discussion of HIV-1 entry and transmission, and drug-resistant phenotypes. Finally, we will assess the methods used in previous and current research to characterize these phenotypes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1253661</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1253661</link>
        <title><![CDATA[Dolutegravir resistance in sub-Saharan Africa: should resource-limited settings be concerned for future treatment?]]></title>
        <pubdate>2023-09-25T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Doreen Kamori</author><author>Godfrey Barabona</author>
        <description><![CDATA[In sub-Saharan Africa (SSA) the burden of non-nucleoside reverse transcriptase inhibitor (NNRTI) HIV drug resistance (HIVDR) has been high over the years. Therefore, in 2018 the World Health Organization (WHO) recommended a regimen based on a integrase strand transfer inhibitor (INSTI), dolutegravir, as the default first-line antiretroviral therapy (ART) in countries in SSA. The scale-up of DTG-based regimens in SSA has gained significant momentum since 2018 and has continued to expand across multiple countries in recent years. However, whether or not the DTG robustness experienced in the developed world will also be achieved in SSA settings is still an important question. Evidence generated from in vitro and in vivo studies suggests that the emergence of DTG HIVDR is HIV-1 subtype dependent. These findings demonstrate that the extensive HIV-1 diversity in SSA can influence DTG effectiveness and the emergence of drug resistance. In addition, the programmatic approach to the transition to DTG adopted by many countries in the SSA region potentially exposes individuals to DTG functional monotherapy, which is associated with the emergence of DTG resistance. In this mini review, we describe the current trends of the effectiveness of DTG as reflected by viral suppression and DTG resistance. Furthermore, we explore how HIV-1 diversity and the programmatic approach in SSA could shape DTG effectiveness and DTG HIVDR in the region.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1225818</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1225818</link>
        <title><![CDATA[Mixed viral infection constrains the genome formula of multipartite cucumber mosaic virus]]></title>
        <pubdate>2023-09-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dieke Boezen</author><author>Maritta Vermeulen</author><author>Marcelle L. Johnson</author><author>René A. A. van der Vlugt</author><author>Carolyn M. Malmstrom</author><author>Mark P. Zwart</author>
        <description><![CDATA[Many plant viruses have a multipartite organization, with multiple genome segments packaged into separate virus particles. The genome formula describes the relative frequencies of all viral genome segments, and previous work suggests rapid changes in these frequencies facilitate virus adaptation. Many studies have reported mixed viral infections in plants, often resulting in strong virus–virus interactions. Here, we tested whether mixed infections with tripartite alfalfa mosaic virus (AMV) and monopartite potato virus Y (PVY) affected the genome formula of the tripartite cucumber mosaic virus (CMV), our experimental model. We found that the CMV titer was reduced in mixed infections with its tripartite Bromoviridae relative AMV and in triple infections with both AMV and PVY, indicating notable virus–virus interactions. The variability of the CMV genome formula was significantly lower in mixed infections (CMV and AMV, CMV and PVY, and CMV and AMV and PVY) than in single infections (CMV only). These observations led to the surprising conclusion that mixed infections with two distinct viruses constrain the CMV genome formula. It remains unclear how common these effects are for different combinations of virus species and strains and what the underlying mechanisms are. We, therefore, extended a simulation model to consider three putative scenarios in which a second virus affected the genome formula. The simulation results also suggested that shifts in the genome formula occur, but may not be widespread due to the required conditions. One scenario modeled—co-infection exclusion through niche differentiation—was congruent with the experimental data, as this scenario led to reductions in genome formula variability and titer of the multipartite virus. Whereas previous studies highlighted host–species effects, our results indicate that the genome formula is also affected by mixed infections, suggesting that there is a broader set of environmental cues that affect the genome formula.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1221156</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1221156</link>
        <title><![CDATA[Phylogenomic and population genetics analyses of extant tomato yellow leaf curl virus strains on a global scale]]></title>
        <pubdate>2023-07-25T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Wendy G. Marchant</author><author>Habibu Mugerwa</author><author>Saurabh Gautam</author><author>Hamed Al-Aqeel</author><author>Jane E. Polston</author><author>Gabriel Rennberger</author><author>Hugh Smith</author><author>Bill Turechek</author><author>Scott Adkins</author><author>Judith K. Brown</author><author>Rajagopalbabu Srinivasan</author>
        <description><![CDATA[Tomato yellow leaf curl virus (TYLCV) is a monopartite DNA virus with a genome size of ~ 2,800 base pairs. The virus belongs to the genus Begomovirus within the family Geminiviridae. Extant TYLCV strains are differentiated based on an established threshold of 94% genome-wide pairwise nucleotide identity. The phylogenetic relationships, diversification mechanisms, including recombination, and extent of spread within and from the center of origin for TYLCV have been reported in previous studies. However, the evolutionary relationships among strains, strains’ distribution and genomic diversification, and genetic mechanisms shaping TYLCV strains’ evolution have not been re-evaluated to consider globally representative genome sequences in publicly available sequence database, including herein newly sequenced genomes from the U.S. and Middle East, respectively. In this study, full-length genome sequences for the extant strains and isolates of TYLCV (n=818) were downloaded from the GenBank database. All previously published genome sequences, and newly sequenced TYLCV genomes of TYLCV isolates from Kuwait and USA, determined herein (n=834), were subjected to recombination analysis. To remove the ‘phylogenetic noise’ imparted by interspecific recombination, the recombinant genomes were removed from the data set, and the remaining non-recombinant genome sequences (n=423) were subjected to population genetics and Bayesian analyses. Results of the phylogeographical analysis indicated that the type strain, TYLCV-Israel, and TYLCV-Mild strain, were globally distributed, spanning Africa, America, Asia, Australia/Oceania, Europe, and New Caledonia, while the other TYLCV strains were prevalent only throughout the Middle East. The results of Bayesian evolutionary (ancestral) analysis predicted that TYLCV-Israel represents the oldest, most recent common ancestor (MRCA) (41,795 years), followed by TYLCV-Mild at 39,808 years. These were closely followed by two Iranian strains viz., TYLCV-Kerman and TYLCV-Iran at 37,529 and 36,420 years, respectively. In contrast, the most recently evolving strains were TYLCV-Kuwait and TYLCV-Kahnooj at 12,445 and 298 years, respectively. Results of the neutrality test indicated that TYLCV-Israel and TYLCV-Mild populations are undergoing purifying selection and/or population expansion, although statistically significant selection was documented for only TYLCV-Israel, based on positive selection acting on five codons.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1158703</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1158703</link>
        <title><![CDATA[The emergence of the Omicron XBB.1.5 variant in India: a brief report on clinical presentation of a few cases]]></title>
        <pubdate>2023-06-02T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Jasmine Samal</author><author>Arjun Bhugra</author><author>Varun Suroliya</author><author>Pramod Gautam</author><author>Reshu Agarwal</author><author>Chhagan Bihari</author><author>Ekta Gupta</author>
        <description><![CDATA[Despite the three years spent navigating the COVID-19 pandemic, scientists are still having to react to the disease due to the constant evolution of novel variants/subvariants. Over the last few months, a global plummet in COVID-19 cases has suggested we are transitioning towards endemic COVID-19. However, the new omicron offshoots (XBB variants) are driving a new surge of cases around the world. A few preliminary research findings suggest that the XBB.1.5 subvariant is more immune-evasive and displays higher binding to ACE2 human receptor than its other related omicron subvariants in circulation. In this first-of-its-kind report, we discuss a few XBB.1.5 cases and its clinical characteristics reported in Delhi State, North India.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1215709</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1215709</link>
        <title><![CDATA[Editorial: Predicting virus evolution: from genome evolution to epidemiological trends]]></title>
        <pubdate>2023-05-19T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Mark P. Zwart</author><author>Anne Kupczok</author><author>Jaime Iranzo</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1156012</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1156012</link>
        <title><![CDATA[Co-detection of respiratory syncytial virus with other respiratory viruses across all age groups before and during the COVID-19 pandemic]]></title>
        <pubdate>2023-03-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Haya Hayek</author><author>Justin Z. Amarin</author><author>Yasmeen Z. Qwaider</author><author>Asim Khanfar</author><author>Tess Stopczynski</author><author>Jonathan Schmitz</author><author>James D. Chappell</author><author>Jesse O. Wrenn</author><author>Andrew J. Spieker</author><author>Natasha B. Halasa</author><author>Leigh M. Howard</author>
        <description><![CDATA[BackgroundPatterns of respiratory syncytial virus (RSV) co-detection with other viruses may have been disrupted during the coronavirus disease 2019 (COVID-19) pandemic, but the clinical impact of viral co-detections with RSV is not well-established. We aimed to explore the frequency and clinical outcomes associated with RSV single detection and co-detection before and during the pandemic.MethodsWe conducted a single-center retrospective cohort study of all children and adults with respiratory samples tested using a respiratory pathogen panel (RPP; 01/01/2018–11/30/2022), a provider-ordered polymerase chain reaction–based assay that detects respiratory pathogens. We stratified our cohort into age groups: 0–4, 5–17, 18–64, and ≥65 years old. Among RSV-positive samples, we compared the proportion of samples with single RSV detection before and during the pandemic and the patterns of specific viral co-detections. We compared the odds of hospitalization, oxygen use, intensive care unit admission, and intubation between individuals with RSV single detection and those with co-detection.ResultsAmong 57,940 samples collected during the study period, 3,986 (6.9%) were RSV-positive. RSV was co-detected with at least one other virus in 1,231/3,158 (39.0%), 104/348 (29.9%), 49/312 (15.7%), and 21/168 (12.5%) of samples from individuals 0–4, 5–17, 18–64, and ≥65 years old, respectively. The relative frequencies of RSV single detection and co-detection were comparable before and during the pandemic except in children 0–4 years old, in whom single RSV detections were more prevalent before (63.7%) than during (59.5%) the pandemic (p=0.021). In children 0–4 years old, RSV co-detection was associated with lower odds of hospitalization compared to single RSV detection, and RSV co-detection with parainfluenza viruses or human rhinovirus/enterovirus was associated with significantly lower odds of hospitalization, while RSV/SARS-CoV-2 co-detection was associated with higher odds of ICU admission. In adults ≥65 years old, RSV co-detection was associated with lower odds of oxygen use.ConclusionThe proportion of RSV co-detection did not appreciably vary before and during the pandemic, except in young children, though the combinations of co-detected viruses did vary. Our findings suggest that the clinical impact of RSV co-detection with other viruses may be age-associated and virus-specific.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2023.1066147</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2023.1066147</link>
        <title><![CDATA[Detecting punctuated evolution in SARS-CoV-2 over the first year of the pandemic]]></title>
        <pubdate>2023-02-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kevin Surya</author><author>Jacob D. Gardner</author><author>Chris L. Organ</author>
        <description><![CDATA[The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) evolved slowly over the first year of the Coronavirus Disease 19 (COVID-19) pandemic with differential mutation rates across lineages. Here, we explore how this variation arose. Whether evolutionary change accumulated gradually within lineages or during viral lineage branching is unclear. Using phylogenetic regression models, we show that ~13% of SARS-CoV-2 genomic divergence up to May 2020 is attributable to lineage branching events (punctuated evolution). The net number of branching events along lineages predicts ~5% of the deviation from the strict molecular clock. We did not detect punctuated evolution in SARS-CoV-1, possibly due to the small sample size, and in sarbecovirus broadly, likely due to a different evolutionary process altogether. Punctuation in SARS-CoV-2 is probably neutral because most mutations were not positively selected and because the strength of the punctuational effect remained constant over time, at least until May 2020, and across continents. However, the small punctuational contribution to SARS-CoV-2 diversity is consistent with the founder effect arising from narrow transmission bottlenecks. Therefore, punctuation in SARS-CoV-2 may represent the macroevolutionary consequence (rate variation) of a microevolutionary process (transmission bottleneck).]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2022.1064882</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2022.1064882</link>
        <title><![CDATA[In-depth genetic characterization of the SARS-CoV-2 pandemic in a two-year frame in North Macedonia using second and third generation sequencing technologies]]></title>
        <pubdate>2023-01-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Maja Vukovikj</author><author>Golubinka Boshevska</author><author>Elizabeta Janchevska</author><author>Teodora Buzharova</author><author>Ardian Preshova</author><author>Milica Simova</author><author>Aneta Peshnacka</author><author>Dragan Kocinski</author><author>Gordana Kuzmanovska</author><author>Shaban Memeti</author><author>Icko Gjorgoski</author>
        <description><![CDATA[The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has a persistent negative impact on both the public health and the global economy. To comprehend the origin, transmission routes and discover the mutations that alter the virus’s transmissibility and pathogenicity, full-length SARS-CoV-2 genomes have to be molecularly characterized. Focusing on a two-year time frame (2020-2021), we provide an in-depth virologic and epidemiological overview of the SARS-CoV-2 pandemic in the Republic of North Macedonia by assessing the frequency and distribution of the circulating SARS-CoV-2 variants. Using genetic characterization and phylogenetic analysis we shed light on the molecular evolution of the virus as well as test for a possible connection between specific SARS-CoV-2 haplotypes and the severity of the clinical symptoms. Our results show that one fifth (21.51%) of the tested respiratory samples for SARS-CoV-2 were positive. A noticeable trend in the incidence and severity of the COVID-19 infections was observed in the 60+ age group between males and females. Of the total number of positive cases, the highest incidence of SARS-CoV-2 was noticed in 60+ males (4,170.4/100,000), with a statistically significant (0,0001) difference between the two sexes. Additionally, a 1.8x increase in male mortality and consequentially significantly higher number of death cases was observed compared to females of the same age group (0.001). A total of 327 samples were sequenced in the period March 2020 - August 2021, showing the temporal distribution of SARS-CoV-2 variants circulating in North Macedonia. The phylogenetic analysis showed that most of the viral genomes were closely related and clustered in four distinctive lineages, B.1, B.1.1.7, B.1.351 and B.1.617.2. A statistically significant difference was observed in the 2C_1 haplotype (p=0.0013), where 10.5% of the patients were hospitalized due to severe clinical condition. By employing genetic sequencing, coupled with epidemiological investigations, we investigated viral distribution patterns, identified emerging variants and detected vaccine breakthrough infections. The present work is the first molecular study giving a comprehensive overview of the genetic landscape of circulating SARS-CoV-2 viruses in North Macedonia in a period of two years.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2022.1077155</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2022.1077155</link>
        <title><![CDATA[Renewed global threat by the novel SARS-CoV-2 variants ‘XBB, BF.7, BQ.1, BA.2.75, BA.4.6’: A discussion]]></title>
        <pubdate>2022-12-23T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Ranjan K. Mohapatra</author><author>Ahmed Mahal</author><author>LV Simhachalam Kutikuppala</author><author>Madhumita Pal</author><author>Venkataramana Kandi</author><author>Ashish K. Sarangi</author><author>Ahmad J. Obaidullah</author><author>Snehasish Mishra</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fviro.2022.1047852</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fviro.2022.1047852</link>
        <title><![CDATA[Corrigendum: Investigating the evolutionary origins of the first three SARS-CoV-2 variants of concern]]></title>
        <pubdate>2022-10-07T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Mahan Ghafari</author><author>Qihan Liu</author><author>Arushi Dhillon</author><author>Aris Katzourakis</author><author>Daniel B. Weissman</author>
        <description></description>
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