scholarly journals PO 8481 HIGH HEPATITIS B VIRUS INCIDENCE AMONG HIV-1-INFECTED TREATMENT-NAIVE ADULTS IN BOTSWANA

2019 ◽  
Vol 4 (Suppl 3) ◽  
pp. A44.1-A44
Author(s):  
Bonolo B Phinius ◽  
Resego Bokete ◽  
Motswedi Anderson ◽  
Tshepiso Mbangiwa ◽  
Wonderful Choga ◽  
...  

BackgroundHepatitis B virus (HBV) is one of the leading causes of death worldwide despite a moderately potent vaccine. HBV prevalence has been shown to be higher in patients infected with the human immunodeficiency virus (HIV), hence increased liver-related morbidity and mortality, as well as general poor health outcomes in HIV-HBV co-infection. We estimated the HBV incidence among HIV-1-infected treatment-naïve adults in a longitudinal cohort in Botswana.MethodsPlasma samples from 200 HIV-1C-infected treatment-naïve participants from a completed longitudinal cohort from 2004 to 2007 were screened for HBV surface antigen (HBsAg). HBsAg was assessed using Murex version 3 enzyme-linked immunosorbent assay as per manufacturer’s instructions at 4 timepoints, 12 months apart. We estimated HBV incidence with 95% confidence interval (CI). Cox proportional regression method was used to estimate hazard ratios [gender, age (≤35 or>35) years, CD4+ T cell count (≤450 or>450) cells/µL and HIV viral load suppression (≤400 or>400) copies/mL].ResultsThe median age of screened individuals was 32 years [Q1, Q3; 28, 40] and 83.5% [167/200] were female. Baseline median CD4+ T cell count was 466.35 cells/µL [Q1, Q3: 380.43, 605.75] and median HIV viral load was 13 450 copies/mL [Q1, Q3: 2365, 37 400]. The HBV incidence was 3.6/100 person-years [95% CI: 2.2–5.6]. There were no significant differences by gender, age, HIV viral load suppression and CD4+ T cell count.ConclusionWe report for the first time a high HBV incidence among HIV-infected adults in Botswana. HBV incidence was high in this population despite generally high CD4 +T cell counts and lower HIV viral loads. Early screening of HBV in HIV-infected individuals is vital and should be included in the national HIV treatment guidelines.

2018 ◽  
Vol 10 (02) ◽  
pp. 162-167
Author(s):  
Sakshee Gupta ◽  
Bharti Malhotra ◽  
Jitendra Kumar Tiwari ◽  
Prabhu Dayal Khandelwal ◽  
Rakesh Kumar Maheshwari

ABSTRACT BACKGROUND: Coinfections of human immunodeficiency virus (HIV) with hepatitis viruses may affect the progress of disease and response to therapy. OBJECTIVES: To study the incidence of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfections in HIV–positive patients and their influence on HIV–1 viral load and cluster of differentiation 4+ (CD4+) T–cell counts. MATERIALS AND METHODS: This pilot study was done on 179 HIV–positive patients attending antiretroviral therapy (ART) centre. Their blood samples were tested for HIV-1 viral load, CD4+ T–cell counts, hepatitis B surface antigen, anti–HCV antibodies, HBV DNA and HCV RNA polymerase chain reaction. RESULTS: Among the 179 patients, 7.82% (14/179) were coinfected with HBV and 4.46% (8/179) with HCV. Median CD4+ T–cell count of HIV monoinfected patients was 200 cells/µl and viral load was 1.67 log10 copies/µl. Median CD4+ T–cell counts of 193 cells/µl for HBV (P = 0.230) and 197 cells/µl for HCV (P = 0.610) coinfected patients were similar to that of HIV monoinfected patients. Viral load was higher in both HBV and HCV infected patients but statistically significant only for HCV (P = 0.017). Increase in CD4+ T–cell counts and decrease in HIV–1 viral load in coinfected patients on 2 years of ART were lower than that in HIV monoinfected patients. CONCLUSION: HBV/HCV coinfected HIV patients had similar CD4+ T–cell counts as in HIV monoinfected patients, higher HIV viral load both in chemo–naive patients and in those on ART as compared to HIV monoinfected patients. However, this study needs to be done on a large scale to assess the impact of coinfection on CD4 count and HIV viral load with proper follow–up of patients every 6 months till at least 2 years.


AIDS ◽  
2012 ◽  
Vol 26 (17) ◽  
pp. 2145-2153 ◽  
Author(s):  
Guangxu Ren ◽  
Stefan Esser ◽  
Christoph Jochum ◽  
Joerg F. Schlaak ◽  
Guido Gerken ◽  
...  

2021 ◽  
Vol 24 (2) ◽  
pp. 109-113
Author(s):  
Florentina Dumitrescu ◽  
◽  
Eugenia-Andreea Marcu ◽  
◽  
◽  
...  

Introduction. Human immunodeficiency virus (HIV) and hepatitis B virus (HBV) are two major causes of death worldwide. These two viruses share routes of transmission, and therefore, HIV–HBV coinfection is common and is associated with low plasma levels of CD4 T lymphocytes and accelerated liver disease progression. Maternal HIV and HBV infections have been individually associated with preterm birth and low birth weight. Case presentation. We describe the case of a 28-year-old patient, 14 weeks pregnant, asymptomatic, who performed Elisa-HIV 1,2 test within prenatal screening, with a positive result, in 2018. From the medical history, we mention that the patient is known for about 5 years with HBV-hepatitis D virus coinfection, for which she underwent interferon treatment for a year. ART was initiated after one month with lamivudine / zidovudine + lopinavir / ritonavir. The patient was adherent to ART (adherence ≥ 95%) during pregnancy. Before birth, the immunovirological evaluation revealed the suppression of maternal HIV viral load, a moderate degree of immunosuppression and undetectable HBV-DNA. The patient gave birth by caesarean section to a female child, with a gestational age of 36 weeks, birth weight of 1730 g, lenght = 43 cm, head circumference = 30 cm, APGAR score = 8 points. The child received antiretroviral prophylaxis with retrovir+epivir, human hepatitis B immunoglobulin and was vaccinated against hepatitis B. The newborn was not vertically infected with HIV and HBV. Conclusions. Good adherence to ART during pregnancy has been associated with HIV viral load and HBV-DNA suppression and it led to the birth of a child who has not been infected with HIV or HBV. Maternal HIV-HBV coinfection was a significant risk factor for preterm birth and low birth weight.


2001 ◽  
Vol 276 (38) ◽  
pp. 35435-35443 ◽  
Author(s):  
Marta Gómez-Gonzalo ◽  
Marta Carretero ◽  
Joaquı́n Rullas ◽  
Enrique Lara-Pezzi ◽  
José Aramburu ◽  
...  

Author(s):  
Salman Khan ◽  
Molly Madan

Objective:- Hepatitis B is noteworthy medical issues that may include the late continuation of liver cirrhosis and hepatocellular carcinoma. The present study aimed for the detection and diffrentiation of Hepatitis B virus HBsAg inactive non-replicative carriers, HBeAg-positive inactive replicative carriers, active carriers & HBeAg-negative chronic hepatitis B by Real Time PCR and their genotyping Methods: This research conducted on 245 positive for HBsAg, 118 (48.16 %) were male and 127 (51.84%) were female patients, which was performed in central research station labortory of Microbiology at netaji subhash Chandra Bose subharti Medical College and Hospital, Meerut Between march 2016 to November 2017 The sera were separated and screened for HBsAg by ELISA kit. Positive samples for HBsAg were tested for HBeAg ELISA kit and DNA Viral load then sequenced for genotying Results:. Of the 245 HBsAg Positive case 55 (1.12%) were HBeAg positive. In 16 PCR positive and HBV genotyping, In HBsAg inactive Non-Replicative 37.5% (n=6) genotype-B and 6.25% (n=1) genotype-A, In HBeAg inactive Replicative 12.5% (n=2) genotype-B and 12.5% (n=2) genotype-A and In HBeAg Active Chronic Hepatitis B 18.75% (n=3) genotype-B and 12.5% (n=2) genotype-A were detected Conclusions: Management strategy, using HBsAg, HBeAg and HBV DNA viral load, seems adequate for the confirmation and diffrentiation of Hepatitis B virus inactive, active carriers & HBeAg-negative chronic hepatitis B patients and genotype B was more prevalent in comparission to genotype A. Distribution of carriers & genotypes, help physicians to prescribe proper antiviral/interferon therapy according to current genotyping pattern in this region Keywords: Hepatitis B virus, Carrier State, HBsAg, HBeAg, RT-PCR


2015 ◽  
Vol 24 (4) ◽  
pp. 473-479 ◽  
Author(s):  
Mihai Voiculescu

Hepatitis B virus (HBV) infection is a major health problem with an important biological and a significant socio-economic impact all over the world. There is a high pressure to come up with a new and more efficient strategy against HBV infection, especially after the recent success of HCV treatment. Preventing HBV infection through vaccine is currently the most efficient way to decrease HBV-related cirrhosis and liver cancer incidence, as well as the best way to suppress the HBV reservoir. The vaccine is safe and efficient in 80-95% of cases. One of its most important roles is to reduce materno-fetal transmission, by giving the first dose of vaccine in the first 24 hours after birth. Transmission of HBV infection early in life is still frequent, especially in countries with high endemicity.Successful HBV clearance by the host is immune-mediated, with a complex combined innate and adaptive cellular and humoral immune response. Different factors, such as the quantity and the sequence of HBV epitope during processing by dendritic cells and presenting by different HLA molecules or the polymorphism of T cell receptors (TOL) are part of a complex network which influences the final response. A new potential therapeutic strategy is to restore T-cell antiviral function and to improve innate and adaptive immune response by immunotherapeutic manipulation.It appears that HBV eradication is far from being completed in the next decades, and a new strategy against HBV infection must be considered. Abbreviations: ALT: alanine aminotransferase; APC: antigen presenting cells; cccDNA: covalently closed circular DNA; HBIG: hepatitis B immunoglobulin; HbsAg: hepatitis B surface antigen; HBV: hepatitis B virus; HCC: hepatocellular carcinoma; CTL: cytotoxic T lymphocyte; IFN: interferon; NUC: nucleos(t)ide analogues; pg RNA: pre genomic RNA; TLR: toll-like receptors; TOL: T cell receptors.


2004 ◽  
Vol 66 (1) ◽  
pp. 19-22
Author(s):  
Nobuaki CHOSA ◽  
Hitoshi MIYAGUNI ◽  
Shinichiro TSUMORI ◽  
Katsumi OGATA ◽  
Mitsuru SETOYAMA

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tingyan Wang ◽  
David A. Smith ◽  
Cori Campbell ◽  
Jolynne Mokaya ◽  
Oliver Freeman ◽  
...  

Abstract Background Current clinical guidelines recommend treating chronic hepatitis B virus (HBV) infection in a minority of cases, but there are relatively scarce data on evolution or progression of liver inflammation and fibrosis in cases of chronic HBV (CHB) that do not meet treatment criteria. We aimed to assess the impact of TDF on liver disease, and the risk of renal impairment in treated CHB patients in comparison to untreated patients. Methods We studied a longitudinal ethnically diverse CHB cohort in the UK attending out-patient clinics between 2005 and 2018. We examined TDF treatment (vs. untreated) as the main exposure, with HBV DNA viral load (VL), ALT, elastography scores and eGFR as the main outcomes, using paired tests and mixed effects model for longitudinal measurements. Additionally, decline of eGFR during follow-up was quantified within individuals by thresholds based on clinical guidelines. Baseline was defined as treatment initiation for TDF group and the beginning of clinical follow-up for untreated group respectively. Results We included 206 adults (60 on TDF, 146 untreated), with a median ± IQR follow-up duration of 3.3 ± 2.8 years. The TDF group was significantly older (median age 39 vs. 35 years, p = 0.004) and more likely to be male (63% vs. 47%, p = 0.04) compared to the untreated group. Baseline difference between TDF and untreated groups reflected treatment eligibility criteria. As expected, VL and ALT declined significantly over time in TDF-treated patients. Elastography scores normalised during treatment in the TDF group reflecting regression of inflammation and/or fibrosis. However, 6/81 (7.4%) of untreated patients had a progression of fibrosis stage from F0-F1 to F2 or F3. There was no evidence of difference in rates or incidence of renal impairment during follow-up in the TDF vs. untreated group. Conclusions Risk of liver inflammation and fibrosis may be raised in untreated patients compared to those receiving TDF, and TDF may benefit a larger percentage of the CHB population.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Lorena Leticia Peixoto de Lima ◽  
Allysson Quintino Tenório de Oliveira ◽  
Tuane Carolina Ferreira Moura ◽  
Ednelza da Silva Graça Amoras ◽  
Sandra Souza Lima ◽  
...  

Abstract Background The HIV-1 epidemic is still considered a global public health problem, but great advances have been made in fighting it by antiretroviral therapy (ART). ART has a considerable impact on viral replication and host immunity. The production of type I interferon (IFN) is key to the innate immune response to viral infections. The STING and cGAS proteins have proven roles in the antiviral cascade. The present study aimed to evaluate the impact of ART on innate immunity, which was represented by STING and cGAS gene expression and plasma IFN-α level. Methods This cohort study evaluated a group of 33 individuals who were initially naïve to therapy and who were treated at a reference center and reassessed 12 months after starting ART. Gene expression levels and viral load were evaluated by real-time PCR, CD4+ and CD8+ T lymphocyte counts by flow cytometry, and IFN-α level by enzyme-linked immunosorbent assay. Results From before to after ART, the CD4+ T cell count and the CD4+/CD8+ ratio significantly increased (p < 0.0001), the CD8+ T cell count slightly decreased, and viral load decreased to undetectable levels in most of the group (84.85%). The expression of STING and cGAS significantly decreased (p = 0.0034 and p = 0.0001, respectively) after the use of ART, but IFN-α did not (p = 0.1558). Among the markers evaluated, the only markers that showed a correlation with each other were STING and CD4+ T at the time of the first collection. Conclusions ART provided immune recovery and viral suppression to the studied group and indirectly downregulated the STING and cGAS genes. In contrast, ART did not influence IFN-α. The expression of STING and cGAS was not correlated with the plasma level of IFN-α, which suggests that there is another pathway regulating this cytokine in addition to the STING–cGAS pathway.


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