Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br Conclusion br Funding br Availability of data and materia

    2022-01-15


    Conclusion
    Funding
    Availability of data and materials
    Authors' contributions
    Ethics approval and consent to participate
    Consent for publication
    Competing interests
    Introduction Hepatitis C virus (HCV) infection is a global public health problem. An estimated 71.1 million people have HCV infection (Polaris Observatory, 2017). Approximately 80% of HCV-infected individuals develop a life-long chronic infection (Alberti et al., 2005). Chronic HCV infection is a major cause of liver cirrhosis and hepatocellular carcinoma worldwide (Hoshida et al., 2014; WHO, 2004), and the most common medical reason for liver transplantation in the US (Charlton et al., 2011). Owing to similar modes of transmission, HCV and HIV infections often co-occur, especially among people who inject drugs (PWID) and men who have sex with men (MSM). Both groups are considered major reservoirs for HCV infection (Arain and Robaeys, 2014; Fraser et al., 2018; Hoornenborg et al., 2017; Taylor et al., 2013). Although public health prevention measures have effectively reduced occurrence of HIV infection in PWID from 23% in 1994–2000 to 8% in 2010 (CDC, 2012; Lee et al., 2003), prominent outbreaks of HIV infection among PWID continue to reemerge in the US and worldwide (Des Jarlais et al., 2016; Fraser et al., 2018; Wejnert et al., 2016). A recent study shows that nearly 70% of all new diagnoses of HIV infections reported in the US in 2015 were contributed by MSM (Singh et al., 2017), which represents a 28% increase from the level observed in 1994–2000 (Lee et al., 2003). Patients with HIV–HCV co-infection experience more liver-related morbidity and mortality, and a higher overall mortality than patients with HCV mono-infection (Chen et al., 2009; Lo Re 3rd et al., 2014). A high prevalence of HIV–HCV co-infection and its impact on mortality among such CW069 sale groups as PWID and MSM is of major concern to public health (Taylor et al., 2013) (additional information available at: www.cdc.gov/hiv/). In the United States, an increase was recently reported in the rate of acute HCV infection, which was especially large in Central Appalachia (Suryaprasad et al., 2014). There was up to a 364% increase in the number of cases with acute HCV infection among young PWID from 2006 to 2012 (Zibbell et al., 2015). Historically, prevalence of HIV infection in rural regions is very low. However, as the recent explosive outbreak of HIV infection in Indiana showed, this situation may rapidly change when HIV gets introduced to a local PWID network. In this outbreak, a single HIV-1 strain was swiftly transmitted among members of a large PWID community with a high prevalence of HCV infection, resulting in 92.3% of the HIV cases being co-infected with HCV (Peters et al., 2016). This high rate of co-infection indicates that both viruses explore same contact network in this PWID community. Recently, we have developed a novel web-based system, Global Hepatitis Outbreak and Surveillance Technology (GHOST), for the detection of HCV transmission, which analyzes sequences of intra-host variants of the HCV E1/E2-junction genomic region, the hypervariable region 1 (HVR1), obtained by next-generation sequencing (NGS) and automatically generates transmission networks (Longmire et al., 2017). Genetic variation along HVR1 of intra-host HCV variants has been shown to be strongly associated with host gender and ethnicity (Lara et al., 2011a), resistance to interferon (Aurora et al., 2009; Lara and Khudyakov, 2012; Lara et al., 2011a; Lara et al., 2011b; Murray et al., 2013) and stages of HCV infection (Astrakhantseva et al., 2011; Lara et al., 2017). Epistatic connectivity among genomic sites (Campo et al., 2011; Lara and Khudyakov, 2012; Lara et al., 2011b) and proteins (Champeimont et al., 2016) has been linked to HCV viral fitness (Sun et al., 2011), virulence (Lara and Khudyakov, 2012) and rates of fibrosis progression (Lara et al., 2014a). All these findings indicate that many viral traits such as adaptation to host, response to treatment and progression of infection and disease in infected individuals are reflected in genetic heterogeneity of intra-host viral populations and can be used to develop models for enhanced molecular surveillance (Khudyakov, 2012).