Pub Date : 2023-09-26DOI: 10.3389/fviro.2023.1160078
Malowane H. Ngoato, Edina Amponsah-Dacosta, Ntombifuthi Blose, Selokela G. Selabe, Thembeni L. Msibi, Mojakgomo H. Motswaledi, Andrew M. Musyoki
Introduction Reactivation of hepatitis B virus (HBV) infection induced by immunosuppressive cancer therapy is associated with fulminant liver disease and death. While national guidelines recommend HBV screening and antiviral prophylaxis for patients with cancer prior to initiating immunosuppressive therapy, compliance with these measures is unclear. This study characterized the burden of HBV infection among patients diagnosed with gynecological or dermatological cancers, with or without underlying HIV infection, before initiating immunosuppressive therapy. Methods Between 2016 – 2018, we recruited study patients from the Dr George Mukhari Academic Hospital in Tshwane, South Africa. Demographic (age, sex) and clinical data (HIV test results, HIV antiviral regimen, type of cancer) were recorded using a standardized data collection form. All participants were tested for HBV surface antigen (HBsAg), and antibodies to the surface (anti-HBs) and core antigens (anti-HBc). For detection of HBV DNA, a nested polymerase chain reaction was used to amplify polymerase gene fragments which were Sanger-sequenced and analyzed using bioinformatics software. All statistical analyses were performed using R version 4.1.0 (2021-05-18) and R studio version 2022.07.2. Results Study participants were predominantly female (96.3%, 103/107) with a median (IQR) age of 50 (17.5) years. Cervical cancer was the most frequent cancer diagnosis (72%). Over half (52.3%; 56/107) of the participants were HIV positive and all but four (92.9%) on highly active antiretroviral therapy at the time of enrollment. The prevalence of chronic hepatitis B in the study population was 11.2% [95% CI:6.2-19.1], increasing to 14.3% [95% CI:6.8-26.8] in the HIV positive sub-population. The overall prevalence of occult HBV infection was 20% [95% CI:12.8-29.7], 57.9% [95% CI:33.97-78.9] of whom tested negative for all serological markers. Phylogenetic inference showed that all polymerase gene sequences generated in this study were sub-genotype A2. Mutational analysis did not reveal any drug resistance-associated amino acid variations in this study. Conclusion These findings suggest that chronic and occult HBV infections are more prevalent among cancer patients with or without underlying HIV infection compared to what has previously been reported for the general South African population. This underscores the need to scale-up universal HBV serological and molecular screening with timely institution of prophylaxis prior to initiating immunosuppressive cancer therapy.
{"title":"Hepatitis B virus infection in patients presenting for immunosuppressive cancer therapy with and without underlying HIV infection","authors":"Malowane H. Ngoato, Edina Amponsah-Dacosta, Ntombifuthi Blose, Selokela G. Selabe, Thembeni L. Msibi, Mojakgomo H. Motswaledi, Andrew M. Musyoki","doi":"10.3389/fviro.2023.1160078","DOIUrl":"https://doi.org/10.3389/fviro.2023.1160078","url":null,"abstract":"Introduction Reactivation of hepatitis B virus (HBV) infection induced by immunosuppressive cancer therapy is associated with fulminant liver disease and death. While national guidelines recommend HBV screening and antiviral prophylaxis for patients with cancer prior to initiating immunosuppressive therapy, compliance with these measures is unclear. This study characterized the burden of HBV infection among patients diagnosed with gynecological or dermatological cancers, with or without underlying HIV infection, before initiating immunosuppressive therapy. Methods Between 2016 – 2018, we recruited study patients from the Dr George Mukhari Academic Hospital in Tshwane, South Africa. Demographic (age, sex) and clinical data (HIV test results, HIV antiviral regimen, type of cancer) were recorded using a standardized data collection form. All participants were tested for HBV surface antigen (HBsAg), and antibodies to the surface (anti-HBs) and core antigens (anti-HBc). For detection of HBV DNA, a nested polymerase chain reaction was used to amplify polymerase gene fragments which were Sanger-sequenced and analyzed using bioinformatics software. All statistical analyses were performed using R version 4.1.0 (2021-05-18) and R studio version 2022.07.2. Results Study participants were predominantly female (96.3%, 103/107) with a median (IQR) age of 50 (17.5) years. Cervical cancer was the most frequent cancer diagnosis (72%). Over half (52.3%; 56/107) of the participants were HIV positive and all but four (92.9%) on highly active antiretroviral therapy at the time of enrollment. The prevalence of chronic hepatitis B in the study population was 11.2% [95% CI:6.2-19.1], increasing to 14.3% [95% CI:6.8-26.8] in the HIV positive sub-population. The overall prevalence of occult HBV infection was 20% [95% CI:12.8-29.7], 57.9% [95% CI:33.97-78.9] of whom tested negative for all serological markers. Phylogenetic inference showed that all polymerase gene sequences generated in this study were sub-genotype A2. Mutational analysis did not reveal any drug resistance-associated amino acid variations in this study. Conclusion These findings suggest that chronic and occult HBV infections are more prevalent among cancer patients with or without underlying HIV infection compared to what has previously been reported for the general South African population. This underscores the need to scale-up universal HBV serological and molecular screening with timely institution of prophylaxis prior to initiating immunosuppressive cancer therapy.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"63 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135719306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-25DOI: 10.3389/fviro.2023.1253661
Doreen Kamori, Godfrey Barabona
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.
{"title":"Dolutegravir resistance in sub-Saharan Africa: should resource-limited settings be concerned for future treatment?","authors":"Doreen Kamori, Godfrey Barabona","doi":"10.3389/fviro.2023.1253661","DOIUrl":"https://doi.org/10.3389/fviro.2023.1253661","url":null,"abstract":"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.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135864646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-22DOI: 10.3389/fviro.2023.1288953
Samuel Ken-En Gan, E. Kostaki
{"title":"Editorial: Methods in bioinformatic and predictive virology","authors":"Samuel Ken-En Gan, E. Kostaki","doi":"10.3389/fviro.2023.1288953","DOIUrl":"https://doi.org/10.3389/fviro.2023.1288953","url":null,"abstract":"","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139337603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cotton blue disease from Africa and its de facto relationship with cotton leafroll dwarf virus: a misleading etiological discrepancy","authors":"Connor Ferguson, Akhtar Ali","doi":"10.3389/fviro.2023.1253174","DOIUrl":"https://doi.org/10.3389/fviro.2023.1253174","url":null,"abstract":"OPINION article Front. Virol., 20 September 2023Sec. Emerging and Reemerging Viruses Volume 3 - 2023 | https://doi.org/10.3389/fviro.2023.1253174","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136314997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-07DOI: 10.3389/fviro.2023.1225818
Dieke Boezen, Maritta Vermeulen, Marcelle L. Johnson, René A. A. van der Vlugt, Carolyn M. Malmstrom, M. Zwart
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.
{"title":"Mixed viral infection constrains the genome formula of multipartite cucumber mosaic virus","authors":"Dieke Boezen, Maritta Vermeulen, Marcelle L. Johnson, René A. A. van der Vlugt, Carolyn M. Malmstrom, M. Zwart","doi":"10.3389/fviro.2023.1225818","DOIUrl":"https://doi.org/10.3389/fviro.2023.1225818","url":null,"abstract":"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.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41615181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-29DOI: 10.3389/fviro.2023.1163385
Neale J Harrison, L. Richardson, Chiara Pallini, I. Morano, Elizabeth Jinks, Jamie Cowley, Hujo Chan, Harriet J. Hill, A. Tuekprakhon, Zhi Li, Cristina Matas de las Heras, A. Teodósio, Andrea Lavado, Robert Moring, A. Ashraf, T. Dafforn, D. Grammatopoulos, J. Gordon, Catherine A. Brady, L. Young, N. Barnes, Z. Stamataki, O. Qureshi
The engagement of the SARS-CoV-2 spike protein with ACE2 is a critical step for viral entry to human cells, and, therefore, blocking this interaction is a major determinant of the efficacy of monoclonal antibody therapeutics and vaccine elicited serum antibodies. The emergence of SARS-CoV-2 variants has necessitated the development of adaptable assays that can be applied to assess the effectiveness of antibody-based therapeutics.Through the testing of a range of recombinant spike proteins, we have developed a cell-based, ACE2/spike protein interaction assay that characterises monoclonal anti-spike protein antibodies and neutralising antibodies in donor serum. The assay uses high-content imaging to quantify cell-bound spike protein fluorescence.Using spike proteins from the original “Wuhan” SARS-CoV-2 strain and the Delta and Omicron variants, we identified differential blocking activity of three monoclonal antibodies directed against the spike receptor-binding domain. Importantly, biological activity in the spike interaction assay translated to efficacy in a SARS-CoV-2 infection assay.The spike protein interaction assay can be used to monitor anti-spike antibodies against the major known SARS-CoV-2 variants and is readily adaptable for quantification of the impact of antibodies against new and emerging SARS-CoV-2 variants.
{"title":"A cell-based, SARS-CoV-2 spike protein interaction assay to inform the neutralising capacity of recombinant and patient sera antibodies","authors":"Neale J Harrison, L. Richardson, Chiara Pallini, I. Morano, Elizabeth Jinks, Jamie Cowley, Hujo Chan, Harriet J. Hill, A. Tuekprakhon, Zhi Li, Cristina Matas de las Heras, A. Teodósio, Andrea Lavado, Robert Moring, A. Ashraf, T. Dafforn, D. Grammatopoulos, J. Gordon, Catherine A. Brady, L. Young, N. Barnes, Z. Stamataki, O. Qureshi","doi":"10.3389/fviro.2023.1163385","DOIUrl":"https://doi.org/10.3389/fviro.2023.1163385","url":null,"abstract":"The engagement of the SARS-CoV-2 spike protein with ACE2 is a critical step for viral entry to human cells, and, therefore, blocking this interaction is a major determinant of the efficacy of monoclonal antibody therapeutics and vaccine elicited serum antibodies. The emergence of SARS-CoV-2 variants has necessitated the development of adaptable assays that can be applied to assess the effectiveness of antibody-based therapeutics.Through the testing of a range of recombinant spike proteins, we have developed a cell-based, ACE2/spike protein interaction assay that characterises monoclonal anti-spike protein antibodies and neutralising antibodies in donor serum. The assay uses high-content imaging to quantify cell-bound spike protein fluorescence.Using spike proteins from the original “Wuhan” SARS-CoV-2 strain and the Delta and Omicron variants, we identified differential blocking activity of three monoclonal antibodies directed against the spike receptor-binding domain. Importantly, biological activity in the spike interaction assay translated to efficacy in a SARS-CoV-2 infection assay.The spike protein interaction assay can be used to monitor anti-spike antibodies against the major known SARS-CoV-2 variants and is readily adaptable for quantification of the impact of antibodies against new and emerging SARS-CoV-2 variants.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45662914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-17DOI: 10.3389/fviro.2023.1232906
Mikako Hirohama, S. Yamashita, Masamitsu N. Asaka, Takahiro Kuroki, Atsushi Kawaguchi
The influenza virus genome consists of single-stranded RNAs and forms viral ribonucleoprotein (RNP) complexes. After viral genome replication in the nucleus, the viral RNP interacts with viral protein M1. The M1-viral RNP complex is exported to the cytoplasm via the CRM1-dependent pathway using NS2/NEP as an export adaptor protein. NEP is a 14 kDa protein and diffusely localizes in the nucleus and cytoplasm. Upon binding to the NLS motif of M1, NEP inhibits the nuclear accumulation of M1 and promotes the nuclear export of M1-viral RNP complex. However, the detail mechanism by which NEP binds to M1 only in the nucleus remains unclear.To visualize the interaction of NEP with M1 in the formation of vRNP export complexes, we performed in situ proximity ligation assays. The close proximity of N-terminal and C-terminal domains of NEP was tested by split Renilla luciferase complementation assays in which the N-terminal and C-terminal fragments of Renilla luciferase were fused to the N-terminus and C-terminus of NEP, respectively.We found that the intramolecular interaction of NEP inhibits the interaction of NEP with M1. The intramolecular interaction of NEP was mediated through the interaction of the N-terminal NES motif with the M1-binding domain at the C-terminus. By adding leptomycin B, a potent inhibitor of CRM1, the interaction of NEP with M1 was impaired. These results suggest that CRM1 disrupts the intramolecular interaction of NEP by recognizing the NES motif at the N-terminus of NEP, thereby promoting the interaction of NEP with M1. We also found that NEP mutant deficient in the intramolecular interaction was co-localized with M1 at the plasma membrane and did not show nuclear localization with M1. Based on these results, we propose that the intramolecular interaction of NEP regulated by CRM1 ensures the unidirectional transport of M1.
{"title":"Intramolecular interaction of NEP regulated by CRM1 ensures the unidirectional transport of M1 for the nuclear export of influenza viral ribonucleoprotein","authors":"Mikako Hirohama, S. Yamashita, Masamitsu N. Asaka, Takahiro Kuroki, Atsushi Kawaguchi","doi":"10.3389/fviro.2023.1232906","DOIUrl":"https://doi.org/10.3389/fviro.2023.1232906","url":null,"abstract":"The influenza virus genome consists of single-stranded RNAs and forms viral ribonucleoprotein (RNP) complexes. After viral genome replication in the nucleus, the viral RNP interacts with viral protein M1. The M1-viral RNP complex is exported to the cytoplasm via the CRM1-dependent pathway using NS2/NEP as an export adaptor protein. NEP is a 14 kDa protein and diffusely localizes in the nucleus and cytoplasm. Upon binding to the NLS motif of M1, NEP inhibits the nuclear accumulation of M1 and promotes the nuclear export of M1-viral RNP complex. However, the detail mechanism by which NEP binds to M1 only in the nucleus remains unclear.To visualize the interaction of NEP with M1 in the formation of vRNP export complexes, we performed in situ proximity ligation assays. The close proximity of N-terminal and C-terminal domains of NEP was tested by split Renilla luciferase complementation assays in which the N-terminal and C-terminal fragments of Renilla luciferase were fused to the N-terminus and C-terminus of NEP, respectively.We found that the intramolecular interaction of NEP inhibits the interaction of NEP with M1. The intramolecular interaction of NEP was mediated through the interaction of the N-terminal NES motif with the M1-binding domain at the C-terminus. By adding leptomycin B, a potent inhibitor of CRM1, the interaction of NEP with M1 was impaired. These results suggest that CRM1 disrupts the intramolecular interaction of NEP by recognizing the NES motif at the N-terminus of NEP, thereby promoting the interaction of NEP with M1. We also found that NEP mutant deficient in the intramolecular interaction was co-localized with M1 at the plasma membrane and did not show nuclear localization with M1. Based on these results, we propose that the intramolecular interaction of NEP regulated by CRM1 ensures the unidirectional transport of M1.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"108 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41277207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-14DOI: 10.3389/fviro.2023.1270008
S. Zúñiga, Jennifer A. Corcoran
{"title":"Editorial: Post-transcriptional regulation of viral protein expression and function","authors":"S. Zúñiga, Jennifer A. Corcoran","doi":"10.3389/fviro.2023.1270008","DOIUrl":"https://doi.org/10.3389/fviro.2023.1270008","url":null,"abstract":"","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42404855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-02DOI: 10.3389/fviro.2023.1253524
A. Adachi, T. Koma, Masako Nomaguchi
{"title":"Editorial: HIV/SIV basic research update","authors":"A. Adachi, T. Koma, Masako Nomaguchi","doi":"10.3389/fviro.2023.1253524","DOIUrl":"https://doi.org/10.3389/fviro.2023.1253524","url":null,"abstract":"","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45451692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-25DOI: 10.3389/fviro.2023.1221156
Wendy G. Marchant, H. Mugerwa, Saurabh Gautam, H. Al-Aqeel, J. Polston, G. Rennberger, Hugh Smith, Bill Turechek, S. Adkins, Judith K. Brown, R. Srinivasan
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.
{"title":"Phylogenomic and population genetics analyses of extant tomato yellow leaf curl virus strains on a global scale","authors":"Wendy G. Marchant, H. Mugerwa, Saurabh Gautam, H. Al-Aqeel, J. Polston, G. Rennberger, Hugh Smith, Bill Turechek, S. Adkins, Judith K. Brown, R. Srinivasan","doi":"10.3389/fviro.2023.1221156","DOIUrl":"https://doi.org/10.3389/fviro.2023.1221156","url":null,"abstract":"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.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48807059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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