Pub Date : 2022-01-01Epub Date: 2021-07-07DOI: 10.1159/000517717
Li Zhu, Yunwen Zhang, Zhengrong Yang, Baisheng Li, Tiejian Feng, Xuan Zou, Jianfan He, Taiping He, Junling Li, Ning Liu, Wei Li, Xiaohui Wang
Objective: The aim of the study was to analyze the relationship between serum antibody and neutralizing antibody titers in convalescent coronavirus disease 2019 (COVID-19) patients with different disease severities, and the seropositive reaction rates of 9 reported B-cell epitopes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Methods: Serum IgG and total antibody titers of 165 convalescent COVID-19 patients were determined by chemiluminescence, the serum neutralization antibody titers were determined by microneutralization assay, and the S/CO values of 9 peptides were detected by indirect enzyme-linked immunosorbent assay. Correlations between the aforementioned indexes were statistically analyzed, and differences in patients with different diseases severities were evaluated.
Results: IgG, total antibody, and neutralizing antibody titers increased with disease severity. The positive rate of the receptor-binding region (RBD) was 100%, and the average positive rate for all the 9 peptides was above 50% in 165 patients. IDf showed the highest rate of positivity (86.06%), with a rate of 95% for the (IDf + IDa) pattern. Moreover, S/CO values of RBD and mix (IDh) were significantly correlated with IgG, total antibody titers, and neutralizing antibody titers (p < 0.001), whereas the S/CO values for other 8 peptides showed no obvious correlation.
Conclusion: In this study, a large sample was used to confirm that the peptide IDf had a high positive reaction rate for all patients (86.06%) and also had the highest detection rate in asymptomatic patients (86.67%). Only long peptide and mixed peptide showed correlation with neutralizing antibody titers, suggesting that the ability of SARS-CoV-2 antibody to neutralize virus infectivity may require the interaction of multiple sites.
{"title":"Seropositive Reaction Rates of 9 B-Cell Epitopes of the SARS-CoV-2 Spike Protein and the Relationship between the Epitopes and Neutralizing Antibody.","authors":"Li Zhu, Yunwen Zhang, Zhengrong Yang, Baisheng Li, Tiejian Feng, Xuan Zou, Jianfan He, Taiping He, Junling Li, Ning Liu, Wei Li, Xiaohui Wang","doi":"10.1159/000517717","DOIUrl":"https://doi.org/10.1159/000517717","url":null,"abstract":"<p><strong>Objective: </strong>The aim of the study was to analyze the relationship between serum antibody and neutralizing antibody titers in convalescent coronavirus disease 2019 (COVID-19) patients with different disease severities, and the seropositive reaction rates of 9 reported B-cell epitopes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).</p><p><strong>Methods: </strong>Serum IgG and total antibody titers of 165 convalescent COVID-19 patients were determined by chemiluminescence, the serum neutralization antibody titers were determined by microneutralization assay, and the S/CO values of 9 peptides were detected by indirect enzyme-linked immunosorbent assay. Correlations between the aforementioned indexes were statistically analyzed, and differences in patients with different diseases severities were evaluated.</p><p><strong>Results: </strong>IgG, total antibody, and neutralizing antibody titers increased with disease severity. The positive rate of the receptor-binding region (RBD) was 100%, and the average positive rate for all the 9 peptides was above 50% in 165 patients. IDf showed the highest rate of positivity (86.06%), with a rate of 95% for the (IDf + IDa) pattern. Moreover, S/CO values of RBD and mix (IDh) were significantly correlated with IgG, total antibody titers, and neutralizing antibody titers (p < 0.001), whereas the S/CO values for other 8 peptides showed no obvious correlation.</p><p><strong>Conclusion: </strong>In this study, a large sample was used to confirm that the peptide IDf had a high positive reaction rate for all patients (86.06%) and also had the highest detection rate in asymptomatic patients (86.67%). Only long peptide and mixed peptide showed correlation with neutralizing antibody titers, suggesting that the ability of SARS-CoV-2 antibody to neutralize virus infectivity may require the interaction of multiple sites.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 1","pages":"29-36"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000517717","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39161438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-08-26DOI: 10.1159/000517057
Seon-Ju Yeo, Vui Thi Hoang, Tuan Bao Duong, Ngoc Minh Nguyen, Hien Thi Tuong, Mudsser Azam, Haan Woo Sung, Hyun Park
Introduction: The avian influenza (AI) virus causes a highly contagious disease which is common in wild and domestic birds and sporadic in humans. Mutations and genetic reassortments among the 8 negative-sense RNA segments of the viral genome alter its pathogenic potential, demanding well-targeted, active surveillance for infection control.
Methods: Wild duck fecal samples were collected during the 2018 bird health annual surveillance in South Korea for tracking variations of the AI virus. One low-pathogenic avian influenza H5N3 reassortment virus (A/mallard duck/South Korea/KNU18-91/2018 [H5N3]) was isolated and genomically characterized by phylogenetic and molecular analyses in this study.
Results: It was devoid of polybasic amino acids at the hemagglutinin (HA) cleavage site and exhibited a stalk region without deletion in the neuraminidase (NA) gene and NA inhibitor resistance-linked E/D627K/N and D701N marker mutations in the PB2 gene, suggesting its low-pathogenic AI. It showed a potential of a reassortment where only HA originated from the H5N3 poultry virus of China and other genes were derived from Mongolia. In phylogenetic analysis, HA was different from that of the isolate of H5N3 in Korea, 2015. In addition, this novel virus showed adaptation in Madin-Darby canine kidney cells, with 8.05 ± 0.14 log10 50% tissue culture infectious dose (TCID50) /mL at 36 h postinfection. However, it could not replicate in mice well, showing positive growth at 3 days postinfection (dpi) (2.1 ± 0.13 log10 TCID50/mL) but not at 6 dpi.
Conclusions: The HA antigenic relationship of A/mallard duck/South Korea/KNU18-91/2018 (H5N3) showed differences toward one of the old low-pathogenic H5N3 viruses in Korea. These results indicated that a novel reassortment low-pathogenic avian influenza H5N3 subtype virus emerged in South Korea in 2018 via novel multiple reassortments with Eurasian viruses, rather than one of old Korean H5N3 strains.
{"title":"Emergence of a Novel Reassortant H5N3 Avian Influenza Virus in Korean Mallard Ducks in 2018.","authors":"Seon-Ju Yeo, Vui Thi Hoang, Tuan Bao Duong, Ngoc Minh Nguyen, Hien Thi Tuong, Mudsser Azam, Haan Woo Sung, Hyun Park","doi":"10.1159/000517057","DOIUrl":"https://doi.org/10.1159/000517057","url":null,"abstract":"<p><strong>Introduction: </strong>The avian influenza (AI) virus causes a highly contagious disease which is common in wild and domestic birds and sporadic in humans. Mutations and genetic reassortments among the 8 negative-sense RNA segments of the viral genome alter its pathogenic potential, demanding well-targeted, active surveillance for infection control.</p><p><strong>Methods: </strong>Wild duck fecal samples were collected during the 2018 bird health annual surveillance in South Korea for tracking variations of the AI virus. One low-pathogenic avian influenza H5N3 reassortment virus (A/mallard duck/South Korea/KNU18-91/2018 [H5N3]) was isolated and genomically characterized by phylogenetic and molecular analyses in this study.</p><p><strong>Results: </strong>It was devoid of polybasic amino acids at the hemagglutinin (HA) cleavage site and exhibited a stalk region without deletion in the neuraminidase (NA) gene and NA inhibitor resistance-linked E/D627K/N and D701N marker mutations in the PB2 gene, suggesting its low-pathogenic AI. It showed a potential of a reassortment where only HA originated from the H5N3 poultry virus of China and other genes were derived from Mongolia. In phylogenetic analysis, HA was different from that of the isolate of H5N3 in Korea, 2015. In addition, this novel virus showed adaptation in Madin-Darby canine kidney cells, with 8.05 ± 0.14 log10 50% tissue culture infectious dose (TCID50) /mL at 36 h postinfection. However, it could not replicate in mice well, showing positive growth at 3 days postinfection (dpi) (2.1 ± 0.13 log10 TCID50/mL) but not at 6 dpi.</p><p><strong>Conclusions: </strong>The HA antigenic relationship of A/mallard duck/South Korea/KNU18-91/2018 (H5N3) showed differences toward one of the old low-pathogenic H5N3 viruses in Korea. These results indicated that a novel reassortment low-pathogenic avian influenza H5N3 subtype virus emerged in South Korea in 2018 via novel multiple reassortments with Eurasian viruses, rather than one of old Korean H5N3 strains.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 1","pages":"1-16"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8820440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39348391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Colorectal cancer is the third most common cancer all over the world, so in the battle to fight this hurdle, new therapeutic approaches such as oncolytic viruses (OV) have attracted much attention because of the fact that they can inherently kill cancer cells. Oncolytic reovirus is one of the candidates for treatment as a nonpathogenic species specially reovirus type 3 Dearing (T3D), which can induce apoptosis. To speed up the entry and function of the reovirus, low-intensity ultrasound, which is a safe system for damage to the cells and tissues, is a promising approach to be used in combination with other therapeutic approach.
Methods: L929 and CT26 cells were infected with reovirus T3D and were exposed to ultrasonic irradiation (1 MHz, 1 W/cm2, and 20% duty factor) for 10 s. The viruses' titer level of both groups was calculated in 2 types of cells by using the CCID50 method and compared with each other. Apoptosis, after 24 h, was measured by the flow cytometry method.
Result: The results of CCID50 in infected cells were exposed to low-intensity ultrasound showed an increased virus titer compared with unexposed infected cells. Moreover, according to the results of the flow cytometry test, it was found that the amount of apoptosis in infected cells that are exposed to low-intensity ultrasound waves is higher than those infected cells.
Conclusion: Due to the results of CCID50 and flow cytometry tests, low-intensity ultrasound increases the cytotoxicity level of reovirus in CT26 cells of the cellular colorectal cancer model.
{"title":"Low-Intensity Ultrasound as a Novel Strategy to Improve the Cytotoxic Effect of Oncolytic Reovirus on Colorectal Cancer Model Cells.","authors":"Negar Sharifi, Hoorieh Soleimanjahi, Manijeh Mokhtari-Dizaji, Razieh Sadat Banijamali, Maliheh Elhamipour, Hesam Karimi","doi":"10.1159/000519492","DOIUrl":"https://doi.org/10.1159/000519492","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer is the third most common cancer all over the world, so in the battle to fight this hurdle, new therapeutic approaches such as oncolytic viruses (OV) have attracted much attention because of the fact that they can inherently kill cancer cells. Oncolytic reovirus is one of the candidates for treatment as a nonpathogenic species specially reovirus type 3 Dearing (T3D), which can induce apoptosis. To speed up the entry and function of the reovirus, low-intensity ultrasound, which is a safe system for damage to the cells and tissues, is a promising approach to be used in combination with other therapeutic approach.</p><p><strong>Methods: </strong>L929 and CT26 cells were infected with reovirus T3D and were exposed to ultrasonic irradiation (1 MHz, 1 W/cm2, and 20% duty factor) for 10 s. The viruses' titer level of both groups was calculated in 2 types of cells by using the CCID50 method and compared with each other. Apoptosis, after 24 h, was measured by the flow cytometry method.</p><p><strong>Result: </strong>The results of CCID50 in infected cells were exposed to low-intensity ultrasound showed an increased virus titer compared with unexposed infected cells. Moreover, according to the results of the flow cytometry test, it was found that the amount of apoptosis in infected cells that are exposed to low-intensity ultrasound waves is higher than those infected cells.</p><p><strong>Conclusion: </strong>Due to the results of CCID50 and flow cytometry tests, low-intensity ultrasound increases the cytotoxicity level of reovirus in CT26 cells of the cellular colorectal cancer model.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 2","pages":"110-118"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39406361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-08-26DOI: 10.1159/000517539
Jie Wei, Yan Sun, Ting-Ting Wang, Gui Zhu, Wan-Hong Liu, Xiao-Hua He, Zhi Li
Background: For foamy virus, the transactivator of spumaretrovirus (Tas) could bind directly to target DNA sequences termed as Tas responsive elements and trigger the viral internal promoter (IP) and long terminal repeat (LTR) promoters. The cellular endogenous factors also play an important role in viral gene expressions. We hypothesized that except the viral transcription factor Tas, the cellular endogenous factors also affect the viral gene expression.
Methods: The full length of the prototype foamy virus (PFV) genome (U21247) was used to predict the potential binding sites of the transcription factors by online software JASPAR (http://jaspar.genereg.net) and Softberry (http://linux1.softberry.com/berry.phtml?topic=index&group=programs&subgroup=promoter). The Dual-Luciferase® Reporter Assay System (Promega, USA) was used to confirm the relative luciferase activities of the test groups. The different representative activating agents or inhibitors of each canonical signal pathway were used to identify the impact of these pathways on PFV 5'LTR and IP promoters.
Results: The results showed different cellular endogenous factors might have respective effects on PFV 5'LTR and IP. It is worth mentioning that activator protein-1 and BCL2-associated athanogene 3, 2 kinds of vital proteins associated with NF-κB and PKC pathways, could activate the basal activity of 5'LTR and IP promoters but inhibit the Tas-regulated activity of both promoters. Furthermore, PFV Tas was identified to trigger the transcription of the NF-κB promoter.
Conclusion: NF-κB had a negative effect on PFV 5'LTR and IP promoter activities, the PKC pathway might upregulate 5'LTR and IP promoter activities, and the JNK and NF-AT signal pathway could increase the Tas-regulated promoter activity of PFV 5'LTR. This study sheds light on the interaction between PFV and the host cell and may help utilize the viral promoters in retroviral vectors designed for gene transfer experiments.
{"title":"The Regulation of Prototype Foamy Virus 5'Long Terminal Repeats and Internal Promoter by Endogenous Transcription Factors.","authors":"Jie Wei, Yan Sun, Ting-Ting Wang, Gui Zhu, Wan-Hong Liu, Xiao-Hua He, Zhi Li","doi":"10.1159/000517539","DOIUrl":"https://doi.org/10.1159/000517539","url":null,"abstract":"<p><strong>Background: </strong>For foamy virus, the transactivator of spumaretrovirus (Tas) could bind directly to target DNA sequences termed as Tas responsive elements and trigger the viral internal promoter (IP) and long terminal repeat (LTR) promoters. The cellular endogenous factors also play an important role in viral gene expressions. We hypothesized that except the viral transcription factor Tas, the cellular endogenous factors also affect the viral gene expression.</p><p><strong>Methods: </strong>The full length of the prototype foamy virus (PFV) genome (U21247) was used to predict the potential binding sites of the transcription factors by online software JASPAR (http://jaspar.genereg.net) and Softberry (http://linux1.softberry.com/berry.phtml?topic=index&group=programs&subgroup=promoter). The Dual-Luciferase® Reporter Assay System (Promega, USA) was used to confirm the relative luciferase activities of the test groups. The different representative activating agents or inhibitors of each canonical signal pathway were used to identify the impact of these pathways on PFV 5'LTR and IP promoters.</p><p><strong>Results: </strong>The results showed different cellular endogenous factors might have respective effects on PFV 5'LTR and IP. It is worth mentioning that activator protein-1 and BCL2-associated athanogene 3, 2 kinds of vital proteins associated with NF-κB and PKC pathways, could activate the basal activity of 5'LTR and IP promoters but inhibit the Tas-regulated activity of both promoters. Furthermore, PFV Tas was identified to trigger the transcription of the NF-κB promoter.</p><p><strong>Conclusion: </strong>NF-κB had a negative effect on PFV 5'LTR and IP promoter activities, the PKC pathway might upregulate 5'LTR and IP promoter activities, and the JNK and NF-AT signal pathway could increase the Tas-regulated promoter activity of PFV 5'LTR. This study sheds light on the interaction between PFV and the host cell and may help utilize the viral promoters in retroviral vectors designed for gene transfer experiments.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 1","pages":"17-28"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8820438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39347577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Host restriction factors are cellular proteins that inhibit specific steps of the viral life cycle. Since the 1970s, several new factors have been identified, including human immunodeficiency virus-1 (HIV-1) replication restriction. Evidence accumulated in the last decade has substantially broadened our understanding of the molecular mechanisms utilized to abrogate the HIV-1 life cycle.
Summary: In this review, we focus on the interaction between host restriction factors participating in the early phase of HIV-1 infection, particularly CA-targeting proteins. Host factors involved in the late phase of the replication cycle, such as viral assembly and egress factors, are also described. Additionally, current reports on well-known antiviral intrinsic factors, as well as other viral restriction factors with their emerging roles, are included.
Conclusion: A comprehensive understanding of the interactions between viruses and hosts is expected to provide insight into the design of novel HIV-1 therapeutic interventions.
{"title":"Updating on Roles of HIV Intrinsic Factors: A Review of Their Antiviral Mechanisms and Emerging Functions.","authors":"Sudarat Hadpech, Sutpirat Moonmuang, Koollawat Chupradit, Umpa Yasamut, Chatchai Tayapiwatana","doi":"10.1159/000519241","DOIUrl":"https://doi.org/10.1159/000519241","url":null,"abstract":"<p><strong>Background: </strong>Host restriction factors are cellular proteins that inhibit specific steps of the viral life cycle. Since the 1970s, several new factors have been identified, including human immunodeficiency virus-1 (HIV-1) replication restriction. Evidence accumulated in the last decade has substantially broadened our understanding of the molecular mechanisms utilized to abrogate the HIV-1 life cycle.</p><p><strong>Summary: </strong>In this review, we focus on the interaction between host restriction factors participating in the early phase of HIV-1 infection, particularly CA-targeting proteins. Host factors involved in the late phase of the replication cycle, such as viral assembly and egress factors, are also described. Additionally, current reports on well-known antiviral intrinsic factors, as well as other viral restriction factors with their emerging roles, are included.</p><p><strong>Conclusion: </strong>A comprehensive understanding of the interactions between viruses and hosts is expected to provide insight into the design of novel HIV-1 therapeutic interventions.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 2","pages":"67-79"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9153338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39370607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-09-28DOI: 10.1159/000519848
Edwige T Yelemkoure, Albert T Yonli, Hermann K Sombie, Issoufou Tao, Abdou Azaque Zouré, Abdoul Karim Ouattara, Abel P Sorgho, Arsène W Zongo, Moctar T A Zeba, Isabelle T Kiendrebeogo, Prosper Bado, Madeleine K Kabré, Théodora M Zohoncon, Florencia W Djigma, Dorcas Obiri-Yeboah, Jacques Simpore
Introduction: Hepatitis C virus (HCV) infection remains a major public health problem worldwide. In Burkina Faso, nearly 720,000 people are living with HCV, and each year about 900 people die from complications of cirrhosis or hepatocellular carcinoma. This study was planned to determine the HCV seroprevalence, characterize circulating genotypes, and monitor HCV viral loads in patients under treatment with antivirals.
Methods: A total of 4,124 individuals and 167 patients in the pre-therapy program were recruited. The "SD Bioline HCV" kit was used for rapid screening of anti-HCV antibodies. Viral load and genotyping were performed in 167 HCV patients on antivirals using the "Iontek HCV Quant" and "Iontek genotyping" kits.
Results: Prevalence of HCV was 1.65% (68/4,124), and the median viral load of participants was 5.37 log10/mL (1.32-7.67 log10/mL). Genotype 2 was predominant with a frequency of 86.23% (144/167) and appeared to be more active with higher viral load compared to 13.77% (23/167) for genotype 1 (p < 0.001). After 24 weeks of pan-genotypic direct-acting antivirals, such as sofosbuvir/daclatasvir and sofosbuvir/velpatasvir, the viral loads of all patients became undetectable.
Conclusion: The responses to antivirals by the circulating genotypes indicate that the results are very satisfactory. Therefore, the prevalence of HCV in the population can be reduced through identification of cases and treatment.
{"title":"Seroprevalence, Genotyping, and Monitoring of Hepatitis C Viral Loads in Patients on Antivirals in Burkina Faso.","authors":"Edwige T Yelemkoure, Albert T Yonli, Hermann K Sombie, Issoufou Tao, Abdou Azaque Zouré, Abdoul Karim Ouattara, Abel P Sorgho, Arsène W Zongo, Moctar T A Zeba, Isabelle T Kiendrebeogo, Prosper Bado, Madeleine K Kabré, Théodora M Zohoncon, Florencia W Djigma, Dorcas Obiri-Yeboah, Jacques Simpore","doi":"10.1159/000519848","DOIUrl":"https://doi.org/10.1159/000519848","url":null,"abstract":"<p><strong>Introduction: </strong>Hepatitis C virus (HCV) infection remains a major public health problem worldwide. In Burkina Faso, nearly 720,000 people are living with HCV, and each year about 900 people die from complications of cirrhosis or hepatocellular carcinoma. This study was planned to determine the HCV seroprevalence, characterize circulating genotypes, and monitor HCV viral loads in patients under treatment with antivirals.</p><p><strong>Methods: </strong>A total of 4,124 individuals and 167 patients in the pre-therapy program were recruited. The \"SD Bioline HCV\" kit was used for rapid screening of anti-HCV antibodies. Viral load and genotyping were performed in 167 HCV patients on antivirals using the \"Iontek HCV Quant\" and \"Iontek genotyping\" kits.</p><p><strong>Results: </strong>Prevalence of HCV was 1.65% (68/4,124), and the median viral load of participants was 5.37 log10/mL (1.32-7.67 log10/mL). Genotype 2 was predominant with a frequency of 86.23% (144/167) and appeared to be more active with higher viral load compared to 13.77% (23/167) for genotype 1 (p < 0.001). After 24 weeks of pan-genotypic direct-acting antivirals, such as sofosbuvir/daclatasvir and sofosbuvir/velpatasvir, the viral loads of all patients became undetectable.</p><p><strong>Conclusion: </strong>The responses to antivirals by the circulating genotypes indicate that the results are very satisfactory. Therefore, the prevalence of HCV in the population can be reduced through identification of cases and treatment.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 3","pages":"151-159"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9501785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39466105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2022-02-14DOI: 10.1159/000522577
Roya Kianfar, Mehrdad Ravanshad, Mohammad Adel Ghiass, Nastaran Rafiee, Ali Shayeghpour, Ali Maleki
Introduction: Epstein-Barr virus (EBV/HHV-4) has been implicated in the pathogenesis of multiple sclerosis (MS). This study was conducted to investigate the levels of pro-inflammatory cytokines IL-1β and IL-6 in healthy EBV carriers and MS patients with prior EBV infection in response to treatment with EBV nuclear antigen 1 (EBNA-1) and replication and transcription activator (BRLF-1/Rta) peptide antigens in whole blood cell culture to assess the cytokine expression across all cells in the peripheral blood.
Methods: Isolated whole blood cells from the included participants were incubated at a concentration of 106 cells/mL with BRLF-1 or EBNA-1. The amount of IL-1β and IL-6 transcripts were measured with quantitative RT-PCR at day 3 after incubation. MTT assay was conducted to examine cytotoxicity of the peptides and their effect on cell viability. Changes in cytokine expression and cell viability were analyzed using one-way and two-way ANOVA, respectively.
Results: Ten MS patients and ten healthy donors were enrolled in the study. Treatment with the peptide antigens resulted in increased cytokines expression in both MS patients and healthy subjects. Furthermore, IL-1β levels were higher in MS patients compared to healthy EBV carriers. MTT assay revealed no significant difference in cell viability between the two groups.
Discussion: The higher levels of IL-1β in response to EBV antigens in MS patients may reflect the host neuroinflammatory environment and support the notion that immune response against EBV has a role as an aggravating factor in the progression of MS by contributing to the neuroinflammatory cascade.
{"title":"Evaluation of IL-1β and IL-6 Expression following EBNA-1 and BRLF-1 Peptide Treatment in Epstein-Barr Virus-Positive Multiple Sclerosis Patients.","authors":"Roya Kianfar, Mehrdad Ravanshad, Mohammad Adel Ghiass, Nastaran Rafiee, Ali Shayeghpour, Ali Maleki","doi":"10.1159/000522577","DOIUrl":"10.1159/000522577","url":null,"abstract":"<p><strong>Introduction: </strong>Epstein-Barr virus (EBV/HHV-4) has been implicated in the pathogenesis of multiple sclerosis (MS). This study was conducted to investigate the levels of pro-inflammatory cytokines IL-1β and IL-6 in healthy EBV carriers and MS patients with prior EBV infection in response to treatment with EBV nuclear antigen 1 (EBNA-1) and replication and transcription activator (BRLF-1/Rta) peptide antigens in whole blood cell culture to assess the cytokine expression across all cells in the peripheral blood.</p><p><strong>Methods: </strong>Isolated whole blood cells from the included participants were incubated at a concentration of 106 cells/mL with BRLF-1 or EBNA-1. The amount of IL-1β and IL-6 transcripts were measured with quantitative RT-PCR at day 3 after incubation. MTT assay was conducted to examine cytotoxicity of the peptides and their effect on cell viability. Changes in cytokine expression and cell viability were analyzed using one-way and two-way ANOVA, respectively.</p><p><strong>Results: </strong>Ten MS patients and ten healthy donors were enrolled in the study. Treatment with the peptide antigens resulted in increased cytokines expression in both MS patients and healthy subjects. Furthermore, IL-1β levels were higher in MS patients compared to healthy EBV carriers. MTT assay revealed no significant difference in cell viability between the two groups.</p><p><strong>Discussion: </strong>The higher levels of IL-1β in response to EBV antigens in MS patients may reflect the host neuroinflammatory environment and support the notion that immune response against EBV has a role as an aggravating factor in the progression of MS by contributing to the neuroinflammatory cascade.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 3","pages":"144-150"},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9501781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39614696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2022-09-09DOI: 10.1159/000525807
Peipei Pan, Jiaohui Li, Wei Lin, Guangyan Long
Introduction: Hepatitis B virus (HBV) infection is a disease with high incidence and lack of effective treatment. In this study, we further explored the mechanism of resveratrol (RVT) in the inhibition of HBV replication. The effects of RVT on HBV replication were verified using in vitro and in vivo experiments.
Methods: HepG2 and HepG2.2.15 cell lines were cultured in vitro, and different concentrations of RVT were used to determine its effect on the proliferation of the two cell lines. Autophagy agonists and inhibitors were given, and whether RVT exerts its effect on the proliferation of HepG2 and HepG2.2.15 cells through autophagy was determined. Reverse transcription-quantitative polymerase chain reaction and Western blot were used to detect changes in autophagy-related factors LC3-II, LC3-I, Beclin 1, and p62. Through transfection of pmiR-155, shmiR-155, and the corresponding control group, the relevant mechanism of RVT in inhibiting the proliferation of HepG2 and HepG2.2.15 cells was analyzed. RVT inhibited the toxicity for HepG2.2.15 cells and reduced HBV replication in vitro (p < 0.05). This effect of RVT was enhanced by rapamycin (RAPA; autophagy activator; p < 0.05) but was partially reversed by 3-MA (autophagy inhibitor; p < 0.05). In addition, our results showed that miR-155 expression was higher in HepG2.2.15 cells than in HepG cells (p < 0.05). miR-155 expression in the RVT treatment group was significantly reduced (p < 0.05). We designed an miR-155 overexpression plasmid, low miR-155 expression plasmid, and the corresponding negative control for transfection and found that transfection of pmiR-155 can partially reverse the effect of RVT (p < 0.05), while transfection with shmiR-155 can enhance the effect of RVT (p < 0.05).
Discussion: RVT inhibits miR-155, activates autophagy, inhibits the toxicity for HepG2.2.15 cells, and reduces HBV replication, providing a new research direction for the treatment of HBV infection.
{"title":"Effects of Resveratrol on Hepatitis B Virus Replication: In vitro and in vivo Experiments.","authors":"Peipei Pan, Jiaohui Li, Wei Lin, Guangyan Long","doi":"10.1159/000525807","DOIUrl":"https://doi.org/10.1159/000525807","url":null,"abstract":"<p><strong>Introduction: </strong>Hepatitis B virus (HBV) infection is a disease with high incidence and lack of effective treatment. In this study, we further explored the mechanism of resveratrol (RVT) in the inhibition of HBV replication. The effects of RVT on HBV replication were verified using in vitro and in vivo experiments.</p><p><strong>Methods: </strong>HepG2 and HepG2.2.15 cell lines were cultured in vitro, and different concentrations of RVT were used to determine its effect on the proliferation of the two cell lines. Autophagy agonists and inhibitors were given, and whether RVT exerts its effect on the proliferation of HepG2 and HepG2.2.15 cells through autophagy was determined. Reverse transcription-quantitative polymerase chain reaction and Western blot were used to detect changes in autophagy-related factors LC3-II, LC3-I, Beclin 1, and p62. Through transfection of pmiR-155, shmiR-155, and the corresponding control group, the relevant mechanism of RVT in inhibiting the proliferation of HepG2 and HepG2.2.15 cells was analyzed. RVT inhibited the toxicity for HepG2.2.15 cells and reduced HBV replication in vitro (p < 0.05). This effect of RVT was enhanced by rapamycin (RAPA; autophagy activator; p < 0.05) but was partially reversed by 3-MA (autophagy inhibitor; p < 0.05). In addition, our results showed that miR-155 expression was higher in HepG2.2.15 cells than in HepG cells (p < 0.05). miR-155 expression in the RVT treatment group was significantly reduced (p < 0.05). We designed an miR-155 overexpression plasmid, low miR-155 expression plasmid, and the corresponding negative control for transfection and found that transfection of pmiR-155 can partially reverse the effect of RVT (p < 0.05), while transfection with shmiR-155 can enhance the effect of RVT (p < 0.05).</p><p><strong>Discussion: </strong>RVT inhibits miR-155, activates autophagy, inhibits the toxicity for HepG2.2.15 cells, and reduces HBV replication, providing a new research direction for the treatment of HBV infection.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 4","pages":"206-214"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9677841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33463686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-06-29DOI: 10.1159/000517052
Fei Zhang, Yao Yang, Bingyu Liang, Yuan Yang, Qiuyu Wei, Peijiang Pan, Li Ye, Hao Liang
New kinds of HIV-1 circulating recombinant forms (CRFs) and unique recombinant forms (URFs) earn a great prevalence in China nowadays. In this study, we identified 2 similar URFs (2016GXNNIDU037 and 2019QZLSIDU253) both isolated from intravenous drug users (IDUs) in Guangxi, China. Phylogenetic analysis of the near full-length genome (NFLG) revealed 2 URFs both clustered with CRF01_AE but setting up a monophyletic branch, supporting a high bootstrap value. Bootscan analysis and subregional recombinant analysis found that the NFLG of 2016GXNNIDU037 and 2019QZLSIDU253 were both composed of CRF01_AE and CRF07_BC, with 3 CRF07_BC mosaic segments inserted into CRF01_AE backbones. The CRF01_AE segments of the 2 URFs clustered with a previously reported cluster 2 lineage of CRF01_AE. The 5 recombinant breakpoints of the 2 URFs were quite similar. Distinct from CRF01_AE/CRF07_BC URFs reported before, 2016GXNNIDU037 and 2019QZLSIDU253 are new evidence of a high genetic variety of HIV-1 in Guangxi, which may pose new challenges to HIV-1 prevention and molecular epidemiological surveillance in China.
{"title":"Identification of Two Similar Novel HIV-1 Recombinant Forms (CRF01_AE/CRF07_BC) among Intravenous Drug Users in Guangxi, China.","authors":"Fei Zhang, Yao Yang, Bingyu Liang, Yuan Yang, Qiuyu Wei, Peijiang Pan, Li Ye, Hao Liang","doi":"10.1159/000517052","DOIUrl":"https://doi.org/10.1159/000517052","url":null,"abstract":"<p><p>New kinds of HIV-1 circulating recombinant forms (CRFs) and unique recombinant forms (URFs) earn a great prevalence in China nowadays. In this study, we identified 2 similar URFs (2016GXNNIDU037 and 2019QZLSIDU253) both isolated from intravenous drug users (IDUs) in Guangxi, China. Phylogenetic analysis of the near full-length genome (NFLG) revealed 2 URFs both clustered with CRF01_AE but setting up a monophyletic branch, supporting a high bootstrap value. Bootscan analysis and subregional recombinant analysis found that the NFLG of 2016GXNNIDU037 and 2019QZLSIDU253 were both composed of CRF01_AE and CRF07_BC, with 3 CRF07_BC mosaic segments inserted into CRF01_AE backbones. The CRF01_AE segments of the 2 URFs clustered with a previously reported cluster 2 lineage of CRF01_AE. The 5 recombinant breakpoints of the 2 URFs were quite similar. Distinct from CRF01_AE/CRF07_BC URFs reported before, 2016GXNNIDU037 and 2019QZLSIDU253 are new evidence of a high genetic variety of HIV-1 in Guangxi, which may pose new challenges to HIV-1 prevention and molecular epidemiological surveillance in China.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 1","pages":"58-66"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000517052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39119282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Chronic fatigue syndrome (CFS) is a neurological disease that is accompanied by excessive fatigue or tiredness. There are several reports confirming the association between human herpesvirus 6 (HHV-6) infection and CFS illness. This systematic review and meta-analysis was performed to integrate the information of published studies with regard to this association until May 2021.
Methods: The literature search was based on keywords including "chronic fatigue syndrome and HHV 6," "chronic fatigue syndrome and HHV-6," "chronic fatigue syndrome and HHV6," "chronic fatigue syndrome and Herpes virus 6," and "chronic fatigue syndrome and Herpesvirus6" in MEDLINE (PubMed), Web of Science, and EMBASE.
Results: The literature search identified 17 studies to be included in the systematic review and 11 studies in meta-analysis. The symmetry funnel plot and Egger's test (p value = 0.2) identified no publication bias among studies. Moreover, the low level of I2 revealed homogeneity across studies.
Discussion: In conclusion, the association between the HHV-6 infection and CFS incidence was substantiated. However, the results of this study also suggest that further comprehensive studies are needed to solidify the association between HHV-6 and CFS. Future studies should consider additional factors that may have affected the significance of such a correlation.
慢性疲劳综合征(CFS)是一种伴有过度疲劳或疲倦的神经系统疾病。有几份报告证实了人类疱疹病毒6型(HHV-6)感染与慢性疲劳综合症之间的联系。本系统综述和荟萃分析纳入了截至2021年5月已发表的有关该关联的研究信息。方法:基于MEDLINE (PubMed)、Web of Science、EMBASE中的关键词“慢性疲劳综合征与HHV-6”、“慢性疲劳综合征与HHV-6”、“慢性疲劳综合征与HHV6”、“慢性疲劳综合征与疱疹病毒6”、“慢性疲劳综合征与疱疹病毒6”进行文献检索。结果:文献检索确定了17项研究纳入系统评价,11项研究纳入荟萃分析。对称漏斗图和Egger检验(p值= 0.2)未发现研究间存在发表偏倚。此外,低水平的I2显示了研究的同质性。讨论:总之,HHV-6感染与CFS发病率之间的关联得到了证实。然而,这项研究的结果也表明,需要进一步的全面研究来巩固HHV-6与CFS之间的联系。未来的研究应考虑可能影响这种相关性重要性的其他因素。
{"title":"Human Herpesvirus 6 Infection and Risk of Chronic Fatigue Syndrome: A Systematic Review and Meta-Analysis.","authors":"Sayed-Hamidreza Mozhgani, Farid Rajabi, Mohsen Qurbani, Yousef Erfani, Somayeh Yaslianifard, Azam Moosavi, Kiomars Pourrostami, Ali Baradaran Bagheri, Alireza Soleimani, Farida Behzadian, Mahshid Safavi, Farhad Rezaei","doi":"10.1159/000517930","DOIUrl":"https://doi.org/10.1159/000517930","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic fatigue syndrome (CFS) is a neurological disease that is accompanied by excessive fatigue or tiredness. There are several reports confirming the association between human herpesvirus 6 (HHV-6) infection and CFS illness. This systematic review and meta-analysis was performed to integrate the information of published studies with regard to this association until May 2021.</p><p><strong>Methods: </strong>The literature search was based on keywords including \"chronic fatigue syndrome and HHV 6,\" \"chronic fatigue syndrome and HHV-6,\" \"chronic fatigue syndrome and HHV6,\" \"chronic fatigue syndrome and Herpes virus 6,\" and \"chronic fatigue syndrome and Herpesvirus6\" in MEDLINE (PubMed), Web of Science, and EMBASE.</p><p><strong>Results: </strong>The literature search identified 17 studies to be included in the systematic review and 11 studies in meta-analysis. The symmetry funnel plot and Egger's test (p value = 0.2) identified no publication bias among studies. Moreover, the low level of I2 revealed homogeneity across studies.</p><p><strong>Discussion: </strong>In conclusion, the association between the HHV-6 infection and CFS incidence was substantiated. However, the results of this study also suggest that further comprehensive studies are needed to solidify the association between HHV-6 and CFS. Future studies should consider additional factors that may have affected the significance of such a correlation.</p>","PeriodicalId":14547,"journal":{"name":"Intervirology","volume":"65 1","pages":"49-57"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000517930","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39275244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}