scholarly journals The Impact of HCV Infection Duration on HIV Disease Progression and Response to cART amongst HIV Seroconverters in the UK

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0132772 ◽  
Author(s):  
Jamie Inshaw ◽  
Clifford Leen ◽  
Martin Fisher ◽  
Richard Gilson ◽  
David Hawkins ◽  
...  
Keyword(s):  
Disease Progression ◽  
Hcv Infection ◽  
Hiv Disease ◽  
The Uk ◽  
The Impact

scholarly journals A Tale of Two Viruses: Immunological Insights Into HCV/HIV Coinfection

2021 ◽  
Vol 12 ◽  
Author(s):  
Samaa T. Gobran ◽  
Petronela Ancuta ◽  
Naglaa H. Shoukry
Keyword(s):  
Disease Progression ◽  
Immune Reconstitution ◽  
Acute Infection ◽  
People Living With Hiv ◽  
Hiv Disease ◽  
Hiv Reservoir ◽  
Cell Counts ◽  
Hiv Coinfection ◽  
Hcv Coinfection ◽  
The Impact

Nearly 2.3 million individuals worldwide are coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV). Odds of HCV infection are six times higher in people living with HIV (PLWH) compared to their HIV-negative counterparts, with the highest prevalence among people who inject drugs (PWID) and men who have sex with men (MSM). HIV coinfection has a detrimental impact on the natural history of HCV, including higher rates of HCV persistence following acute infection, higher viral loads, and accelerated progression of liver fibrosis and development of end-stage liver disease compared to HCV monoinfection. Similarly, it has been reported that HCV coinfection impacts HIV disease progression in PLWH receiving anti-retroviral therapies (ART) where HCV coinfection negatively affects the homeostasis of CD4+ T cell counts and facilitates HIV replication and viral reservoir persistence. While ART does not cure HIV, direct acting antivirals (DAA) can now achieve HCV cure in nearly 95% of coinfected individuals. However, little is known about how HCV cure and the subsequent resolution of liver inflammation influence systemic immune activation, immune reconstitution and the latent HIV reservoir. In this review, we will summarize the current knowledge regarding the pathogenesis of HIV/HCV coinfection, the effects of HCV coinfection on HIV disease progression in the context of ART, the impact of HIV on HCV-associated liver morbidity, and the consequences of DAA-mediated HCV cure on immune reconstitution and HIV reservoir persistence in coinfected patients.

scholarly journals Changes of Gut-Microbiota-Liver Axis in Hepatitis C Virus Infection

Biology ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 55
Author(s):  
Mohammed El-Mowafy ◽  
Abdelaziz Elgaml ◽  
Mohamed El-Mesery ◽  
Salma Sultan ◽  
Tamer A. E. Ahmed ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Gut Microbiota ◽  
Disease Progression ◽  
Disease Status ◽  
Hcv Infection ◽  
Treatment Regimens ◽  
Liver Health ◽  
The Impact ◽  
Gut Microbiota Dysbiosis

The gut–liver-axis is a bidirectional coordination between the gut, including microbial residents, the gut microbiota, from one side and the liver on the other side. Any disturbance in this crosstalk may lead to a disease status that impacts the functionality of both the gut and the liver. A major cause of liver disorders is hepatitis C virus (HCV) infection that has been illustrated to be associated with gut microbiota dysbiosis at different stages of the disease progression. This dysbiosis may start a cycle of inflammation and metabolic disturbance that impacts the gut and liver health and contributes to the disease progression. This review discusses the latest literature addressing this interplay between the gut microbiota and the liver in HCV infection from both directions. Additionally, we highlight the contribution of gut microbiota to the metabolism of antivirals used in HCV treatment regimens and the impact of these medications on the microbiota composition. This review sheds light on the potential of the gut microbiota manipulation as an alternative therapeutic approach to control the liver complications post HCV infection.

scholarly journals Assessing the impact and cost-effectiveness of needle and syringe provision and opioid substitution therapy on hepatitis C transmission among people who inject drugs in the UK: an analysis of pooled data sets and economic modelling

2017 ◽  
Vol 5 (5) ◽  
pp. 1-118 ◽  
Author(s):  
Lucy Platt ◽  
Sedona Sweeney ◽  
Zoe Ward ◽  
Lorna Guinness ◽  
Matthew Hickman ◽  
...  
Keyword(s):  
Cost Effectiveness ◽  
Cost Effective ◽  
Pooled Analysis ◽  
Hcv Infection ◽  
Data Sets ◽  
Opioid Substitution Therapy ◽  
High Coverage ◽  
Impact Modelling ◽  
The Uk ◽  
The Impact

Background There is limited evidence of the impact of needle and syringe programmes (NSPs) and opioid substitution therapy (OST) on hepatitis C virus (HCV) incidence among people who inject drugs (PWID), nor have there been any economic evaluations. Objective(s) To measure (1) the impact of NSP and OST, (2) changes in the extent of provision of both interventions, and (3) costs and cost-effectiveness of NSPs on HCV infection transmission. Design We conducted (1) a systematic review; (2) an analysis of existing data sets, including collating costs of NSPs; and (3) a dynamic deterministic model to estimate the impact of differing OST/NSP intervention coverage levels for reducing HCV infection prevalence, incidence and disease burden, and incremental cost-effectiveness ratios to measure the cost-effectiveness of current NSP provision versus no provision. Setting Cost-effectiveness analysis and impact modelling in three UK sites. The pooled analysis drew on data from the UK and Australia. The review was international. Participants PWID. Interventions NSP coverage (proportion of injections covered by clean needles) and OST. Outcome New cases of HCV infection. Results The review suggested that OST reduced the risk of HCV infection acquisition by 50% [rate ratio (RR) 0.50, 95% confidence interval (CI) 0.40 to 0.63]. Weaker evidence was found in areas of high (≥ 100%) NSP coverage (RR 0.77, 95% CI 0.38 to 1.54) internationally. There was moderate evidence for combined high coverage of NSPs and OST (RR 0.29, 95% CI 0.13 to 0.65). The pooled analysis showed that combined high coverage of NSPs and OST reduced the risk of HCV infection acquisition by 29–71% compared with those on minimal harm reduction (no OST, ≤ 100% NSP coverage). NSPs are likely to be cost-effective and are cost-saving in some settings. The impact modelling suggest that removing OST (current coverage 81%) and NSPs (coverage 54%) in one site would increase HCV infection incidence by 329% [95% credible interval (CrI) 110% to 953%] in 2031 and at least double (132% increase; 95% CrI 51% to 306%) the number of new infections over 15 years. Increasing NSP coverage to 80% has the largest impact in the site with the lowest current NSP coverage (35%), resulting in a 27% (95% CrI 7% to 43%) decrease in new infections and 41% (95% CrI 11% to 72%) decrease in incidence by 2031 compared with 2016. Addressing homelessness and reducing the harm associated with the injection of crack cocaine could avert approximately 60% of HCV infections over the next 15 years. Limitations Findings are limited by the misclassification of NSP coverage and the simplified intervention definition that fails to capture the integrated services that address other social and health needs as part of this. Conclusions There is moderate evidence of the effectiveness of OST and NSPs, especially in combination, on HCV infection acquisition risk. Policies to ensure that NSPs can be accessed alongside OST are needed. NSPs are cost-saving in some sites and cost-effective in others. NSPs and OST are likely to prevent considerable rates of HCV infection in the UK. Increasing NSP coverage will have most impact in settings with low coverage. Scaling up other interventions such as HCV infection treatment are needed to decrease epidemics to low levels in higher prevalence settings. Future work To understand the mechanisms through which NSPs and OST achieve their effect and the optimum contexts to support implementation. Funding The National Institute for Health Research Public Health Research programme.

Clinical and Biological Implications of Hepatitis C Virus Positivity in Waldenstrom's Macroglobulinemia Patients.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2934-2934
Author(s):  
Alessandra Tedeschi ◽  
Eleonora Vismara ◽  
Marzia Varettoni ◽  
Antonino Greco ◽  
Francesca Ricci ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Disease Progression ◽  
Treatment Time ◽  
Conflicts Of Interest ◽  
Hcv Infection ◽  
Hcv Rna ◽  
Neutrophil Granulocytes ◽  
Increased Risk ◽  
The Impact

Abstract Abstract 2934 Poster Board II-910 Background: hepatitis C virus (HCV) infection has been associated with increased risk of developing B-cell lymphoprolipherative disorders through chronic immune stimulation. Discordant data have been reported about the prevalence of HCV infection in patients with Waldenström's Macroglobulinemia (WM) and the putative role of HCV in lymphomagenesis of this non-Hodgkin Lymphoma subtype remains controversial. Aim: the current retrospective study was conducted to assess the impact of this infection itself in the clinical and biological features and outcome among WM patients as compared with those with HCV negative WM. Patients and methods: we analyzed 140 WM patients with tested anti-HCV antibody (HCV-Ab). HCV-Ab positivity was detected in 21 cases (15%). Clinical characteristics of patients at diagnosis of WM are reported in the table below. Results: HCV positivity was correlated to lower counts of platelets, neutrophil granulocytes, haemoglobin and with presence of cryoglobulins or autoantibodies and splenomegaly. Interestingly we even found a strong link between the presence of HCV and serum parameters of tumor burden such as beta-2 microglobulin (B2-M) and lactate dehydrogenase (LDH). Furthermore we did not reveal any outcome implications in terms of disease progression needing treatment, time from diagnosis to first therapy, overall survival between HCV- and HCV+ patients. Overall, 88 patients (63%) received treatment for disease progression with schedules including Rituximab in 46 cases (52% of treated patients). Rituximab was administered even in HCV-RNA positive patients associated to Cyclophosphamide and Fludarabine and this did not translate in hepatitis development. HCV-RNA was strictly monitored during immunotherapy and we did not observe any significant flair. Conclusions: in our series of patients HCV infection does not seem to affect clinical outcome of disease. Moreover, in our experience patients with documented infection can receive the same schedule of treatment including intensive chemotherapy even with monoclonal antibodies without development of further toxicity. Disclosures: No relevant conflicts of interest to declare.

The impact of HIV disease progression on serum lipoproteins

AIDS ◽  
1992 ◽  
Vol 6 (12) ◽  
pp. 1551 ◽  
Author(s):  
J. Meenan ◽  
E. Mooney ◽  
N. Mosquita ◽  
A. H. Johnson ◽  
P. Collins ◽  
...  
Keyword(s):  
Disease Progression ◽  
Hiv Disease ◽  
Serum Lipoproteins ◽  
The Impact

scholarly journals Impact of HLA-B*52:01-Driven Escape Mutations on Viral Replicative Capacity

2020 ◽  
Vol 94 (13) ◽  
Author(s):  
Ming-Han Chloe Tsai ◽  
Supriya Singh ◽  
Emily Adland ◽  
Philip Goulder
Keyword(s):  
Disease Progression ◽  
Significant Loss ◽  
T Cell Response ◽  
Study Cohort ◽  
Replicative Capacity ◽  
Hiv Disease ◽  
Immune Control ◽  
Cd4 Counts ◽  
The Impact ◽  
B 52

ABSTRACT HLA-B*52:01 is strongly associated with protection against HIV disease progression. However, the mechanisms of HLA-B*52:01-mediated immune control have not been well studied. We here describe a cohort with a majority of HIV C-clade-infected individuals from Delhi, India, where HLA-B*52:01 is highly prevalent (phenotypic frequency, 22.5%). Consistent with studies of other cohorts, expression of HLA-B*52:01 was associated with high absolute CD4 counts and therefore a lack of HIV disease progression. We here examined the impact of HLA-B*52:01-associated viral polymorphisms within the immunodominant C clade Gag epitope RMTSPVSI (here, RI8; Gag residues 275 to 282) on viral replicative capacity (VRC) since HLA-mediated reduction in VRC is a central mechanism implicated in HLA-associated control of HIV. We observed in HLA-B*52:01-positive individuals a higher frequency of V280T, V280S, and V280A variants within RI8 (P = 0.0001). Each of these variants reduced viral replicative capacity in C clade viruses, particularly the V280A variant (P < 0.0001 in both the C clade consensus and in the Indian study cohort consensus p24 Gag backbone), which was also associated with significantly higher absolute CD4 counts in the donors (median, 941.5 cells/mm3; P = 0.004). A second HLA-B*52:01-associated mutation, K286R, flanking HLA-B*52:01-RI8, was also analyzed. Although selected in HLA-B*52:01-positive subjects often in combination with the V280X variants, this mutation did not act as a compensatory mutant but, indeed, further reduced VRC. These data are therefore consistent with previous work showing that HLA-B molecules that are associated with immune control of HIV principally target conserved epitopes within the capsid protein, escape from which results in a significant reduction in VRC. IMPORTANCE Few studies have addressed the mechanisms of immune control in HIV-infected subjects in India, where an estimated 2.7 million people are living with HIV. We focus here on a study cohort in Delhi on one of the most prevalent HLA-B alleles, HLA-B*52:01, present in 22.5% of infected individuals. HLA-B*52:01 has consistently been shown in other cohorts to be associated with protection against HIV disease progression, but studies have been limited by the low prevalence of this allele in North America and Europe. Among the C-clade-infected individuals, we show that HLA-B*52:01 is the most protective of all the HLA-B alleles expressed in the Indian cohort and is associated with the highest absolute CD4 counts. Further, we show that the mechanism by which HLA-B*52:01 mediates immune protection is, at least in part, related to the inability of HIV to evade the HLA-B*52:01-restricted p24 Gag-specific CD8+ T-cell response without incurring a significant loss to viral replicative capacity.

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