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    • The lower number of samples

    2022-01-19

    The lower number of samples tested for the comparison between cobas 4800 HIV-1 and RealTime HIV-1, especially at or below 50 copies/mL (Table 6), could limit our ability to discern a difference in the ability of the various assays to identify patients with virological failure. However, the 95% CI around the overall percent agreement between assays are comparable. In conclusion, we have shown that cobas 4800 HIV-1 is highly sensitive, precise and accurate. It provides VL results that are comparable to other commercially available HIV VL assays, based on minimal overall VL quantification differences between platforms within the tests’ dynamic ranges, for all HIV-1 subtypes. The technical benefits of the platform, combined with the accurate measurement of low-level viremia may enable early detection of treatment failure. Detection of treatment failure at low VL may precede the emergence of drug resistance, or be a consequence of it gamma-Glu-Cys [35,36]. Ultimately, automated platforms such as cobas 4800 HIV-1 will allow the scale-up of VL measurement that is required to achieve the “third 90″ of the ambitious UNAIDS 90-90-90 targets.
    Funding Funding for this study including support for third-party writing assistance for this manuscript to Data First Consulting (Belmont, CA, USA) was provided by Roche Molecular Systems, Inc. (Pleasanton, CA, USA).
    Ethical approval
    Competing interests
    Acknowledgements
    Introduction Since the start of the pandemic in the early 1980s, HIV infection has been a major public health crisis across the world. Currently, around 37 million people are infected with HIV, with 1.8 million of them infected in 2016 alone. Although HIV-infection affects every region of the globe, the majority of infections are found in in sub-Saharan Africa and southeast Asia (UNAIDS 2017). Initially a terminal diagnosis, the advent of combinatorial antiretroviral therapy (cART or HAART) in 1996 dramatically improved the prognosis for HIV, enabling infection to be managed as a chronic condition rather than a terminal illness (Saylor, 2016, Heaton, 2011, Rappaport and Volsky, 2015). This therapeutic strategy treated patients with multiple (generally 3) antiretroviral drugs simultaneously, preventing escape mutations within the virus and thereby significantly improving the suppression of HIV replication. Successful cART has lengthened the lifespan and improved the quality of life for infected individuals. However, effects of cART have also created new health issues, as chronic infection and long-term exposure to antiretrovirals have created a suite of new metabolic, cardiovascular and neurologic disorders in infected individuals. Even when HIV replication is fully suppressed with cART, around 50% of infected individuals still display a variety of neuropathological and neurocognitive sequelae known as NeuroHIV, or when referring specifically to the neurocognitive effects, as HIV-associated neurocognitive disorders (HAND) (Saylor, 2016, Heaton, 2010). While severe forms of neurocognitive impairment are rare in the cART era, the prevalence of HAND is increasing, and deficits in executive functioning, working memory, and psychomotor fluency are still frequently observed in HIV patients (Heaton, 2011, Woods, 2010, Melrose, 2008). These can significantly impair therapeutic adherence (Hinkin, 2002) and accelerate the development of peripheral disease (Grant, 2014). The development of these disorders is initiated by HIV infection of the central nervous system (CNS), which occurs in nearly all infected individuals shortly after initial infection (Davis, 1992, Valcour, 2012). Within the CNS, the primary targets for HIV are myeloid lineage cells, such as microglia and perivascular macrophages. Infection of these cells is central to HIV neuropathogenesis, as infected myeloid cells generate new virions to further spread infection, and both infected and uninfected myeloid cells produce inflammatory mediators in response to infection (Koenig, 1986, Navia, 1986, Williams and Hickey, 2002, Kraft-Terry, 2009, Rappaport and Volsky, 2015, Burdo et al., 2013). The persistence of neurocognitive impairment in virally suppressed individuals suggests subclinical alterations in neurotransmission, neuronal and immune function may underlie the earliest manifestations of NeuroHIV in the cART era (Ipser, 2015, Harezlak, 2011, Gelman, 2012, Ernst, 2002, Anderson, 2015, Andersen, 2010, Gelman, 2013).