28 research outputs found

    HIV-1 RNA genital tract shedding after cryotherapy for visual inspection with acetic acid-positive cervical lesions in western Kenya

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    Objectives: To quantify genital tract HIV-1 RNA (GT-HIV RNA) shedding among women living with HIV (WLHIV) before and after cryotherapy treatment for visual inspection with acetic acid (VIA) positive cervical lesions. Methods:We conducted a prospective, longitudinal study of 39 WLHIV on antiretroviral treatment (ART) undergoing cryotherapy for VIA positive lesions in Kenya from 2015-2017. Eligibility for cryotherapy were lesions that covered Results: Detectable GT-HIV RNA was found in 4/39 (10%) participants pre-cryotherapy, 1/30 (3.3%) and 3/26 (11.5%) participants at the 2- and 8-weeks post-cryotherapy, respectively. Only 6/39 (13%) participants had detectable GT-HIV RNA at any point during the study. 2/6 had recent high PVL (range: 49,124-150,695 copies/mL) within 3 months of starting the study and detectable GT-HIV RNA at follow-up visits. 4/6 had undetectable recent PVL within 3-11 months of the study but each had detectable GT-HIV RNA pre-cryotherapy. The mean GT-HIV RNA among 4/39 WLHIV with shedding at pre-cryotherapy was 43,109 (range: 21,812-73,625) copies/mL. Only one participant had GT-HIV RNA (73,125 copies/mL) at 2-weeks post-cryotherapy (N=30); she had no shedding pre-cryotherapy but had a PVL of 49,124 copies/mL 3 months before the study. The mean GT-HIV RNA at 8-weeks post-cryotherapy (N=26) was 44,668 (range: 21,256-64,812) copies/mL among three participants. One of the 3 had high PVL of 150,695 copies/mL 3 months prior to cryotherapy while 2/3 had GT-HIV RNA shedding at baseline despite undetectable most recent PVL. However, their undetectable PVL was 8-11 months prior to cryotherapy which may not accurately reflect PVL at baseline. Conclusions: The majority of GT-HIV RNA shedding was detected before cryotherapy. This finding suggests that cryotherapy was not the primary cause of GT-HIV RNA shedding. Non-adherence to ART might have played a major role. The small sample size and failure to perform paired GT-HIV RNA and PVL tests at each visit are limitations of the study. Further research on the effect of cryotherapy on GT-HIV RNA shedding in ART non-adherent compared to ART-adherent WLHIV is needed

    Human immunodeficiency virus type 1 RNA genital tract shedding after cryotherapy for cervical intraepithelial neoplasia in Western Kenya

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    Abstract :This prospective study of 39 women living with human immunodeficiency virus (HIV) on antiretroviral therapy in Western Kenya aimed to quantify genital tract HIV-1 RNA (GT-HIV RNA) shedding before and after cryotherapy for cervical intraepithelial neoplasia. Most GT-HIV RNA shedding was detected precryotherapy, suggesting that cryotherapy was not the primary cause of shedding

    High number of HPAI H5 virus infections and antibodies in wild carnivores in the Netherlands, 2020-2022

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    In October 2020, a new lineage of a clade 2.3.4.4b HPAI virus of the H5 subtype emerged in Europe, resulting in the largest global outbreak of HPAI to date, with unprecedented mortality in wild birds and poultry. The virus appears to have become enzootic in birds, continuously yielding novel HPAI virus variants. The recently increased abundance of infected birds worldwide increases the probability of bird-mammal contact, particularly in wild carnivores. Here, we performed molecular and serological screening of over 500 dead wild carnivores and sequencing of RNA positive materials. We show virological evidence for HPAI H5 virus infection in 0.8%, 1.4%, and 9.9% of animals tested in 2020, 2021, and 2022 respectively, with the highest proportion of positives in foxes, polecats and stone martens. We obtained near full genomes of 7 viruses and detected PB2 amino acid substitutions known to play a role in mammalian adaptation in three sequences. Infections were also found in without neurological signs or mortality. Serological evidence for infection was detected in 20% of the study population. These findings suggests that a high proportion of wild carnivores is infected but undetected in current surveillance programmes. We recommend increased surveillance in susceptible mammals, irrespective of neurological signs or encephalitis

    Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

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    Highly pathogenic avian influenza (HPAI) viruses of the H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasionally in humans. In recent years, H5 HPAI viruses of this lineage infecting poultry in Asia have spilled over into wild birds and spread via bird migration to countries in Europe, Africa, and North America. In 2016/2017, this spillover resulted in the largest HPAI epidemic on record in Europe and was associated with an unusually high frequency of reassortments between H5 HPAI viruses and cocirculating low-pathogenic avian influenza viruses. Here, we show that the seven main H5 reassortant viruses had various combinations of gene segments 1, 2, 3, 5, and 6. Using detailed time-resolved phylogenetic analysis, most of these gene segments likely originated from wild birds and at dates and locations that corresponded to their hosts' migratory cycles. However, some gene segments in two reassortant viruses likely originated from domestic anseriforms, either in spring 2016 in east China or in autumn 2016 in central Europe. Our results demonstrate that, in addition to domestic anseriforms in Asia, both migratory wild birds and domestic anseriforms in Europe are relevant sources of gene segments for recent reassortant H5 HPAI viruses. The ease with which these H5 HPAI viruses reassort, in combination with repeated spillovers of H5 HPAI viruses into wild birds, increases the risk of emergence of a reassortant virus that persists in wild bird populations yet remains highly pathogenic for poultry
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