Chen Chen, Spencer R. Haupert, Lauren Zimmermann, Xu Shi, L. Fritsche, B. Mukherjee
Abstract Introduction This study aims to examine the worldwide prevalence of post COVID-19 condition, through a systematic review and meta-analysis. Methods PubMed, Embase, and iSearch were searched on July 5, 2021 with verification extending to March 13, 2022. Using a random effects framework with DerSimonian-Laird estimator, we meta-analyzed post COVID-19 condition prevalence at 28+ days from infection. Results 50 studies were included, and 41 were meta-analyzed. Global estimated pooled prevalence of post COVID-19 condition was 0.43 (95% CI: 0.39,0.46). Hospitalized and non-hospitalized patients have estimates of 0.54 (95% CI: 0.44,0.63) and 0.34 (95% CI: 0.25,0.46), respectively. Regional prevalence estimates were Asia— 0.51 (95% CI: 0.37,0.65), Europe— 0.44 (95% CI: 0.32,0.56), and North America— 0.31 (95% CI: 0.21,0.43). Global prevalence for 30, 60, 90, and 120 days after infection were estimated to be 0.37 (95% CI: 0.26,0.49), 0.25 (95% CI: 0.15,0.38), 0.32 (95% CI: 0.14,0.57) and 0.49 (95% CI: 0.40,0.59), respectively. Fatigue was the most common symptom reported with a prevalence of 0.23 (95% CI: 0.17,0.30), followed by memory problems (0.14 [95% CI: 0.10,0.19]). Discussion This study finds post COVID-19 condition prevalence is substantial; the health effects of COVID-19 appear to be prolonged and can exert stress on the healthcare system.
{"title":"Global Prevalence of Post COVID-19 Condition or Long COVID: A Meta-Analysis and Systematic Review","authors":"Chen Chen, Spencer R. Haupert, Lauren Zimmermann, Xu Shi, L. Fritsche, B. Mukherjee","doi":"10.1093/infdis/jiac136","DOIUrl":"https://doi.org/10.1093/infdis/jiac136","url":null,"abstract":"Abstract Introduction This study aims to examine the worldwide prevalence of post COVID-19 condition, through a systematic review and meta-analysis. Methods PubMed, Embase, and iSearch were searched on July 5, 2021 with verification extending to March 13, 2022. Using a random effects framework with DerSimonian-Laird estimator, we meta-analyzed post COVID-19 condition prevalence at 28+ days from infection. Results 50 studies were included, and 41 were meta-analyzed. Global estimated pooled prevalence of post COVID-19 condition was 0.43 (95% CI: 0.39,0.46). Hospitalized and non-hospitalized patients have estimates of 0.54 (95% CI: 0.44,0.63) and 0.34 (95% CI: 0.25,0.46), respectively. Regional prevalence estimates were Asia— 0.51 (95% CI: 0.37,0.65), Europe— 0.44 (95% CI: 0.32,0.56), and North America— 0.31 (95% CI: 0.21,0.43). Global prevalence for 30, 60, 90, and 120 days after infection were estimated to be 0.37 (95% CI: 0.26,0.49), 0.25 (95% CI: 0.15,0.38), 0.32 (95% CI: 0.14,0.57) and 0.49 (95% CI: 0.40,0.59), respectively. Fatigue was the most common symptom reported with a prevalence of 0.23 (95% CI: 0.17,0.30), followed by memory problems (0.14 [95% CI: 0.10,0.19]). Discussion This study finds post COVID-19 condition prevalence is substantial; the health effects of COVID-19 appear to be prolonged and can exert stress on the healthcare system.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"186 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74175250","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}
B. Beddingfield, Lori A Rowe, K. Russell-Lodrigue, Lara A. Doyle-Meyers, Nadia Golden, S. Spencer, N. Chirichella, R. Blair, N. Maness, C. Roy
Abstract Breakthrough gastrointestinal COVID-19 was observed after experimental SARS-CoV-2 upper mucosal infection in a rhesus macaque undergoing low-dose monoclonal antibody prophylaxis. High levels of viral RNA were detected in intestinal sites contrasting with minimal viral replication in upper respiratory mucosa. Sequencing of virus recovered from tissue in 3 gastrointestinal sites and rectal swab revealed loss of furin cleavage site deletions present in the inoculating virus stock and 2 amino acid changes in spike that were detected in 2 colon sites but not elsewhere, suggesting compartmentalized replication and intestinal viral evolution. This suggests suboptimal antiviral therapies promote viral sequestration in these anatomies.
{"title":"Breakthrough Gastrointestinal COVID-19 and Intrahost Evolution Consequent to Combination Monoclonal Antibody Prophylaxis","authors":"B. Beddingfield, Lori A Rowe, K. Russell-Lodrigue, Lara A. Doyle-Meyers, Nadia Golden, S. Spencer, N. Chirichella, R. Blair, N. Maness, C. Roy","doi":"10.1093/infdis/jiac134","DOIUrl":"https://doi.org/10.1093/infdis/jiac134","url":null,"abstract":"Abstract Breakthrough gastrointestinal COVID-19 was observed after experimental SARS-CoV-2 upper mucosal infection in a rhesus macaque undergoing low-dose monoclonal antibody prophylaxis. High levels of viral RNA were detected in intestinal sites contrasting with minimal viral replication in upper respiratory mucosa. Sequencing of virus recovered from tissue in 3 gastrointestinal sites and rectal swab revealed loss of furin cleavage site deletions present in the inoculating virus stock and 2 amino acid changes in spike that were detected in 2 colon sites but not elsewhere, suggesting compartmentalized replication and intestinal viral evolution. This suggests suboptimal antiviral therapies promote viral sequestration in these anatomies.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"305 1","pages":"1588 - 1592"},"PeriodicalIF":0.0,"publicationDate":"2022-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76859962","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}
M. van Wijhe, Caroline K Johannesen, L. Simonsen, I. M. Jørgensen, T. Fischer
AIM Infant respiratory syncytial virus infection (RSV) has been associated with asthma later in life. We explored the risk of recurrent wheeze or asthma in children with infant RSV-associated hospitalization compared to other respiratory infections. METHODS We performed a retrospective cohort study using Danish national hospital discharge registers. Infants under 6 months, born between January 1995 and October 2018, and with a RSV hospital admission were compared to infants hospitalized for injuries, non-RSV acute upper respiratory tract infection (AURTI), pneumonia and other respiratory pathogens, non-pathogen coded lower respiratory tract infections (LRTI), pertussis, or non-specific respiratory infections. Infants were followed until recurrent wheeze or asthma diagnosis, death, migration, age 10 years, or study end. We estimated cumulative incidence rate ratios (CIRR) and hazard ratios (HR) adjusted for sex, age at inclusion, hospital length of stay (LOS), maternal smoking, 5 minute APGAR score (APGAR5), prematurity, and congenital risk factors (CRF). RESULTS We included 68130 infants, of whom 20920 (30.7%) had RSV hospitalization. The cumulative incidence rate of recurrent wheeze or asthma was 16.6 per 1000 person-years after RSV hospitalization, higher than after injury (CIRR: 2.69; 95% CI: 2.48-2.92), AURTI (1.48; 1.34-1.58), or pertussis (2.32; 1.85-2.91), similar to pneumonia and other respiratory pathogens (1.15; 0.99-1.34) and LRTI (0.79; 0.60-1.04), but lower than non-specific respiratory infections (0.79; 0.73-0.87).Adjusted HRs for recurrent wheeze or asthma after RSV hospitalization compared to injuries decreased from 2.37 (95% CI: 2.08-2.70) for 0 to <1 year to 1.23 (0.88-1.73) for 6 to <10 years for term-born children, and from 1.48 (1.09-2.00) to 0.60 (0.25-1.43) for preterm-born children. Sex, maternal smoking, LOS, CRF, and APGAR5 were independent risk factors. CONCLUSIONS Infant RSV hospitalization is associated with recurrent wheeze and asthma hospitalization, predominantly in preschool age. If causal, RSV-prophylaxis, including vaccines, may significantly reduce disease burden of wheeze and asthma.
{"title":"A retrospective cohort study on infant respiratory tract infection hospitalizations and recurrent wheeze and asthma risk: impact of respiratory syncytial virus.","authors":"M. van Wijhe, Caroline K Johannesen, L. Simonsen, I. M. Jørgensen, T. Fischer","doi":"10.1093/infdis/jiac141","DOIUrl":"https://doi.org/10.1093/infdis/jiac141","url":null,"abstract":"AIM\u0000Infant respiratory syncytial virus infection (RSV) has been associated with asthma later in life. We explored the risk of recurrent wheeze or asthma in children with infant RSV-associated hospitalization compared to other respiratory infections.\u0000\u0000\u0000METHODS\u0000We performed a retrospective cohort study using Danish national hospital discharge registers. Infants under 6 months, born between January 1995 and October 2018, and with a RSV hospital admission were compared to infants hospitalized for injuries, non-RSV acute upper respiratory tract infection (AURTI), pneumonia and other respiratory pathogens, non-pathogen coded lower respiratory tract infections (LRTI), pertussis, or non-specific respiratory infections. Infants were followed until recurrent wheeze or asthma diagnosis, death, migration, age 10 years, or study end. We estimated cumulative incidence rate ratios (CIRR) and hazard ratios (HR) adjusted for sex, age at inclusion, hospital length of stay (LOS), maternal smoking, 5 minute APGAR score (APGAR5), prematurity, and congenital risk factors (CRF).\u0000\u0000\u0000RESULTS\u0000We included 68130 infants, of whom 20920 (30.7%) had RSV hospitalization. The cumulative incidence rate of recurrent wheeze or asthma was 16.6 per 1000 person-years after RSV hospitalization, higher than after injury (CIRR: 2.69; 95% CI: 2.48-2.92), AURTI (1.48; 1.34-1.58), or pertussis (2.32; 1.85-2.91), similar to pneumonia and other respiratory pathogens (1.15; 0.99-1.34) and LRTI (0.79; 0.60-1.04), but lower than non-specific respiratory infections (0.79; 0.73-0.87).Adjusted HRs for recurrent wheeze or asthma after RSV hospitalization compared to injuries decreased from 2.37 (95% CI: 2.08-2.70) for 0 to <1 year to 1.23 (0.88-1.73) for 6 to <10 years for term-born children, and from 1.48 (1.09-2.00) to 0.60 (0.25-1.43) for preterm-born children. Sex, maternal smoking, LOS, CRF, and APGAR5 were independent risk factors.\u0000\u0000\u0000CONCLUSIONS\u0000Infant RSV hospitalization is associated with recurrent wheeze and asthma hospitalization, predominantly in preschool age. If causal, RSV-prophylaxis, including vaccines, may significantly reduce disease burden of wheeze and asthma.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"78 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77416432","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}
M. Spatola, C. Loos, D. Cizmeci, Nicholas Webb, M. Gorman, Evan Rossignol, S. Shin, D. Yuan, Laura Fontana, S. Mukerji, D. Lauffenburger, D. Gabuzda, G. Alter
Abstract The central nervous system (CNS) has emerged as a critical HIV reservoir. Thus, interventions aimed at controlling and eliminating HIV must include CNS-targeted strategies. Given the inaccessibility of the brain, efforts have focused on cerebrospinal fluid (CSF), aimed at defining biomarkers of HIV-disease in the CNS, including HIV-specific antibodies. However, how antibodies traffic between the blood and CNS, and whether specific antibody profiles track with HIV-associated neurocognitive disorders (HAND) remains unclear. Here, we comprehensively profiled HIV-specific antibodies across plasma and CSF from 20 antiretroviral therapy (ART) naive or treated persons with HIV. CSF was populated by IgG1 and IgG3 antibodies, with reduced Fc-effector profiles. While ART improved plasma antibody functional coordination, CSF profiles were unaffected by ART and were unrelated to HAND severity. These data point to a functional sieving of antibodies across the blood-brain barrier, providing previously unappreciated insights for the development of next-generation therapeutics targeting the CNS reservoir.
{"title":"Functional Compartmentalization of Antibodies in the Central Nervous System During Chronic HIV Infection","authors":"M. Spatola, C. Loos, D. Cizmeci, Nicholas Webb, M. Gorman, Evan Rossignol, S. Shin, D. Yuan, Laura Fontana, S. Mukerji, D. Lauffenburger, D. Gabuzda, G. Alter","doi":"10.1093/infdis/jiac138","DOIUrl":"https://doi.org/10.1093/infdis/jiac138","url":null,"abstract":"Abstract The central nervous system (CNS) has emerged as a critical HIV reservoir. Thus, interventions aimed at controlling and eliminating HIV must include CNS-targeted strategies. Given the inaccessibility of the brain, efforts have focused on cerebrospinal fluid (CSF), aimed at defining biomarkers of HIV-disease in the CNS, including HIV-specific antibodies. However, how antibodies traffic between the blood and CNS, and whether specific antibody profiles track with HIV-associated neurocognitive disorders (HAND) remains unclear. Here, we comprehensively profiled HIV-specific antibodies across plasma and CSF from 20 antiretroviral therapy (ART) naive or treated persons with HIV. CSF was populated by IgG1 and IgG3 antibodies, with reduced Fc-effector profiles. While ART improved plasma antibody functional coordination, CSF profiles were unaffected by ART and were unrelated to HAND severity. These data point to a functional sieving of antibodies across the blood-brain barrier, providing previously unappreciated insights for the development of next-generation therapeutics targeting the CNS reservoir.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"24 1","pages":"738 - 750"},"PeriodicalIF":0.0,"publicationDate":"2022-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74793535","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":"Economics of Eradication: Counting on the Polio Experience.","authors":"Ananda S. Bandyopadhyay, W. Orenstein","doi":"10.1093/infdis/jiac132","DOIUrl":"https://doi.org/10.1093/infdis/jiac132","url":null,"abstract":"","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80794040","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}
Weijia Xiong, T. Tsang, Ranawaka A.P.M Perera, Nancy H. L. Leung, V. Fang, I. Barr, J. Peiris, B. Cowling
We explored the potential for a biphasic pattern in waning of antibody titers after influenza vaccination. We collected blood samples in a randomized controlled trial of influenza vaccination in children, and tested them with hemagglutination inhibition (HAI) assays for influenza A(H3N2) and influenza B/Victoria lineage. Using piecewise log-linear mixed-effect models, we found evidence for a faster initial waning of antibody titers for the first 1-2 years after vaccination and then slower longer-term declines. Children with higher post-vaccination titers had faster antibody decay.
{"title":"Biphasic waning of hemagglutination inhibition antibody titers after influenza vaccination in children.","authors":"Weijia Xiong, T. Tsang, Ranawaka A.P.M Perera, Nancy H. L. Leung, V. Fang, I. Barr, J. Peiris, B. Cowling","doi":"10.1093/infdis/jiac117","DOIUrl":"https://doi.org/10.1093/infdis/jiac117","url":null,"abstract":"We explored the potential for a biphasic pattern in waning of antibody titers after influenza vaccination. We collected blood samples in a randomized controlled trial of influenza vaccination in children, and tested them with hemagglutination inhibition (HAI) assays for influenza A(H3N2) and influenza B/Victoria lineage. Using piecewise log-linear mixed-effect models, we found evidence for a faster initial waning of antibody titers for the first 1-2 years after vaccination and then slower longer-term declines. Children with higher post-vaccination titers had faster antibody decay.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83422678","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}
K. Louvanto, Prativa Baral, A. Burchell, A. Ramanakumar, M. El-Zein, P. Tellier, F. Coutlée, M. Roger, E. Franco
Abstract Background Human leukocyte antigen (HLA) polymorphism influences innate and adaptive immune responses. Among heterosexual couples in the HPV Infection and Transmission Among Couples Through Heterosexual Activity (HITCH) cohort study, we examined whether allele sharing in a couple predicted the partners’ infections with the same human papillomavirus (HPV) type. Methods We tested genital samples from 271 couples for 36 HPV genotypes by polymerase chain reaction. We used direct DNA sequencing to type HLA-B07, -DRB1, -DQB1 and -G. Generalized estimating equations were used to examine the associations between the extent of allele sharing and HPV type concordance in which at least 1 of the partners was HPV positive. Results We identified 106 different HLA alleles. The most common HLA alleles among couples were G*01:01:01 (95.6%), G*01:01:02 (60.1%), DQB1*03:01 (57.2%), and DRB1*07:01 (46.9%). Allele sharing was as follows: 19.6% shared none, 43.2% shared 1 only, 25.1% shared 2, and 12.5% shared 3–5. Irrespective of HLA class, grouped or in combination, the extent of allele sharing was not a significant predictor of type-specific HPV concordance in a couple (odds ratio, 1.1 [95% confidence interval, .5–2.1], for 3–5 vs none). Conclusions We found no evidence that the extent of HLA allele concordance influences the likelihood of HPV transmission in newly formed heterosexual couples.
{"title":"Role of Human Leukocyte Antigen Allele Sharing in Human Papillomavirus Infection Transmission Among Heterosexual Couples: Findings From the HITCH Cohort Study","authors":"K. Louvanto, Prativa Baral, A. Burchell, A. Ramanakumar, M. El-Zein, P. Tellier, F. Coutlée, M. Roger, E. Franco","doi":"10.1093/infdis/jiac115","DOIUrl":"https://doi.org/10.1093/infdis/jiac115","url":null,"abstract":"Abstract Background Human leukocyte antigen (HLA) polymorphism influences innate and adaptive immune responses. Among heterosexual couples in the HPV Infection and Transmission Among Couples Through Heterosexual Activity (HITCH) cohort study, we examined whether allele sharing in a couple predicted the partners’ infections with the same human papillomavirus (HPV) type. Methods We tested genital samples from 271 couples for 36 HPV genotypes by polymerase chain reaction. We used direct DNA sequencing to type HLA-B07, -DRB1, -DQB1 and -G. Generalized estimating equations were used to examine the associations between the extent of allele sharing and HPV type concordance in which at least 1 of the partners was HPV positive. Results We identified 106 different HLA alleles. The most common HLA alleles among couples were G*01:01:01 (95.6%), G*01:01:02 (60.1%), DQB1*03:01 (57.2%), and DRB1*07:01 (46.9%). Allele sharing was as follows: 19.6% shared none, 43.2% shared 1 only, 25.1% shared 2, and 12.5% shared 3–5. Irrespective of HLA class, grouped or in combination, the extent of allele sharing was not a significant predictor of type-specific HPV concordance in a couple (odds ratio, 1.1 [95% confidence interval, .5–2.1], for 3–5 vs none). Conclusions We found no evidence that the extent of HLA allele concordance influences the likelihood of HPV transmission in newly formed heterosexual couples.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"51 1","pages":"1175 - 1183"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78421488","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}
S. Moon, I. Janssens, K. Kim, B. Stijlemans, S. Magez, M. Radwanska
BACKGROUND Trypanosoma brucei brucei (T. b. brucei) evades host immune responses by multiple means, including the disruption of B cell homeostasis. This hampers anti-trypanosome vaccine development. As the cellular mechanism underlying this pathology has never been addressed, our study focuses on the fate of memory B cells (MBCs) in vaccinated mice upon trypanosome challenge. METHODS A trypanosome variant surface glycoprotein (VSG) and fluorescent phycoerythrin (PE) were used as immunization antigens. Functional and cellular characteristics of antigen-specific MBCs were studied after homologous and heterologous parasite challenge. RESULTS Immunization with AnTat 1.1 VSG triggers a specific antibody response and isotype-switched CD73 +CD273 +CD80 + MBCs, delivering 90% sterile protection against a homologous parasite challenge. As expected, AnTat 1.1 VSG immunization does not protect against infection with heterologous VSG-switched parasites. After successful curative drug treatment, mice were shown to have completely lost their previously induced protective immunity against the homologous parasites, coinciding with the loss of vaccine-induced MBCs. A PE immunization approach confirmed that trypanosome infections cause the general loss of antigen-specific splenic and bone marrow MBCs, and a reduction in antigen-specific IgGs. CONCLUSION Trypanosomosis induces general immunological memory loss. This benefits the parasites by reducing the stringency for antigenic variation requirements.
{"title":"Trypanosoma brucei brucei Infection Depletes Memory B Cells Resulting in Inability of the Host to Recall Protective B Cells Responses.","authors":"S. Moon, I. Janssens, K. Kim, B. Stijlemans, S. Magez, M. Radwanska","doi":"10.1093/infdis/jiac112","DOIUrl":"https://doi.org/10.1093/infdis/jiac112","url":null,"abstract":"BACKGROUND\u0000Trypanosoma brucei brucei (T. b. brucei) evades host immune responses by multiple means, including the disruption of B cell homeostasis. This hampers anti-trypanosome vaccine development. As the cellular mechanism underlying this pathology has never been addressed, our study focuses on the fate of memory B cells (MBCs) in vaccinated mice upon trypanosome challenge.\u0000\u0000\u0000METHODS\u0000A trypanosome variant surface glycoprotein (VSG) and fluorescent phycoerythrin (PE) were used as immunization antigens. Functional and cellular characteristics of antigen-specific MBCs were studied after homologous and heterologous parasite challenge.\u0000\u0000\u0000RESULTS\u0000Immunization with AnTat 1.1 VSG triggers a specific antibody response and isotype-switched CD73 +CD273 +CD80 + MBCs, delivering 90% sterile protection against a homologous parasite challenge. As expected, AnTat 1.1 VSG immunization does not protect against infection with heterologous VSG-switched parasites. After successful curative drug treatment, mice were shown to have completely lost their previously induced protective immunity against the homologous parasites, coinciding with the loss of vaccine-induced MBCs. A PE immunization approach confirmed that trypanosome infections cause the general loss of antigen-specific splenic and bone marrow MBCs, and a reduction in antigen-specific IgGs.\u0000\u0000\u0000CONCLUSION\u0000Trypanosomosis induces general immunological memory loss. This benefits the parasites by reducing the stringency for antigenic variation requirements.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"83 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77646291","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}
Minh Dao Ngo, Stacey Bartlett, H. Bielefeldt-Ohmann, Cheng Xiang Foo, Roma Sinha, Buddhika Jayakody Arachige, Sarah Reed, T. Mandrup-Poulsen, M. Rosenkilde, K. Ronacher
Abstract Background We previously reported that reduced GPR183 expression in blood from tuberculosis (TB) patients with diabetes is associated with more severe TB. Methods To further elucidate the role of GPR183 and its oxysterol ligands in the lung, we studied dysglycemic mice infected with Mycobacterium tuberculosis (Mtb). Results We found upregulation of the oxysterol-producing enzymes CH25H and CYP7B1 and increased concentrations of 25-hydroxycholesterol upon Mtb infection in the lungs of mice. This was associated with increased expression of GPR183 indicative of oxysterol-mediated recruitment of GPR183-expressing immune cells to the lung. CYP7B1 was predominantly expressed by macrophages in TB granulomas. CYP7B1 expression was significantly blunted in lungs from dysglycemic animals, which coincided with delayed macrophage infiltration. GPR183-deficient mice similarly had reduced macrophage recruitment during early infection. Conclusions Taken together, we demonstrate a requirement of the GPR183/oxysterol axis for positioning of macrophages to the site of infection and add an explanation to more severe TB in diabetes patients.
{"title":"A Blunted GPR183/Oxysterol Axis During Dysglycemia Results in Delayed Recruitment of Macrophages to the Lung During Mycobacterium tuberculosis Infection","authors":"Minh Dao Ngo, Stacey Bartlett, H. Bielefeldt-Ohmann, Cheng Xiang Foo, Roma Sinha, Buddhika Jayakody Arachige, Sarah Reed, T. Mandrup-Poulsen, M. Rosenkilde, K. Ronacher","doi":"10.1093/infdis/jiac102","DOIUrl":"https://doi.org/10.1093/infdis/jiac102","url":null,"abstract":"Abstract Background We previously reported that reduced GPR183 expression in blood from tuberculosis (TB) patients with diabetes is associated with more severe TB. Methods To further elucidate the role of GPR183 and its oxysterol ligands in the lung, we studied dysglycemic mice infected with Mycobacterium tuberculosis (Mtb). Results We found upregulation of the oxysterol-producing enzymes CH25H and CYP7B1 and increased concentrations of 25-hydroxycholesterol upon Mtb infection in the lungs of mice. This was associated with increased expression of GPR183 indicative of oxysterol-mediated recruitment of GPR183-expressing immune cells to the lung. CYP7B1 was predominantly expressed by macrophages in TB granulomas. CYP7B1 expression was significantly blunted in lungs from dysglycemic animals, which coincided with delayed macrophage infiltration. GPR183-deficient mice similarly had reduced macrophage recruitment during early infection. Conclusions Taken together, we demonstrate a requirement of the GPR183/oxysterol axis for positioning of macrophages to the site of infection and add an explanation to more severe TB in diabetes patients.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"10 1","pages":"2219 - 2228"},"PeriodicalIF":0.0,"publicationDate":"2022-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84095815","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}
P. G. Choe, Jisu Hong, Jiyoung Park, E. Chang, C. K. Kang, N. Kim, Chang-Han Lee, W. Park, M. Oh
Abstract Background Humoral immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may wane rapidly in persons recovered from mild coronavirus disease 2019 (COVID-19), but little is known about the longevity. Methods Serum samples were obtained 8, 12, and 18 months after infection from 20 patients with mild COVID-19. The binding activities of serum antibodies (IgA, IgG, and IgM) against SARS-CoV-2 antigens of the Wuhan-1 reference strain (wild-type) and the B.1.1.7, P.1, B.1.167.2, and B.1.1.529 variants were measured by enzyme-linked immunosorbent assays. Neutralizing antibody titers were measured using a cytopathic effect-based live virus neutralization assay. Results Serum IgA and IgG antibodies against spike or receptor-binding domain (RBD) protein of wild-type SARS-CoV-2 were detected for up to 18 months, and neutralizing antibodies persisted for 8 to 18 months after infection. However, any significant antibody responses against RBD proteins of SARS-CoV-2 variants were not observed, and median neutralizing antibody titers against the Delta variant at 8, 12, and 18 months were 8–11 fold lower than against wild-type viruses (P < .001). Conclusions Humoral immunity persisted for up to 18 months after SARS-CoV-2 infection in patients with mild COVID-19. Humoral immune activity against more recently circulating variants, however, was reduced in this population.
{"title":"Persistent Antibody Responses up to 18 Months after Mild SARS-CoV-2 Infection","authors":"P. G. Choe, Jisu Hong, Jiyoung Park, E. Chang, C. K. Kang, N. Kim, Chang-Han Lee, W. Park, M. Oh","doi":"10.1093/infdis/jiac099","DOIUrl":"https://doi.org/10.1093/infdis/jiac099","url":null,"abstract":"Abstract Background Humoral immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may wane rapidly in persons recovered from mild coronavirus disease 2019 (COVID-19), but little is known about the longevity. Methods Serum samples were obtained 8, 12, and 18 months after infection from 20 patients with mild COVID-19. The binding activities of serum antibodies (IgA, IgG, and IgM) against SARS-CoV-2 antigens of the Wuhan-1 reference strain (wild-type) and the B.1.1.7, P.1, B.1.167.2, and B.1.1.529 variants were measured by enzyme-linked immunosorbent assays. Neutralizing antibody titers were measured using a cytopathic effect-based live virus neutralization assay. Results Serum IgA and IgG antibodies against spike or receptor-binding domain (RBD) protein of wild-type SARS-CoV-2 were detected for up to 18 months, and neutralizing antibodies persisted for 8 to 18 months after infection. However, any significant antibody responses against RBD proteins of SARS-CoV-2 variants were not observed, and median neutralizing antibody titers against the Delta variant at 8, 12, and 18 months were 8–11 fold lower than against wild-type viruses (P < .001). Conclusions Humoral immunity persisted for up to 18 months after SARS-CoV-2 infection in patients with mild COVID-19. Humoral immune activity against more recently circulating variants, however, was reduced in this population.","PeriodicalId":22572,"journal":{"name":"The Indonesian Journal of Infectious Diseases","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76259784","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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