HIV and SARS-CoV-2 infection in postpartum Kenyan women and their infants

BackgroundHIV may increase SARS-CoV-2 infection risk and COVID-19 severity generally, but data are limited about its impact on postpartum women and their infants. As such, we characterized SARS-CoV-2 infection among mother-infant pairs in Nairobi, Kenya. MethodsWe conducted a nested study of 53 HIV-uninfected and 51 healthy women living with HIV, as well as their HIV-exposed uninfected (N=41) and HIV-unexposed (N=48) infants, participating in a prospective cohort. SARS-CoV-2 serology was performed on plasma collected between 1 May-31 December 2020 to determine the incidence, risk factors, and symptoms of infection. SARS-CoV-2 RNA PCR and sequencing was also performed on stool samples from seropositive participants. ResultsSARS-CoV-2 seropositivity was found in 38% of the 104 mothers and in 17% of the 89 infants. There was no significant association between SARS-CoV-2 infection and maternal HIV (Hazard Ratio [HR]=1.51, 95% CI: 0.780-2.94) or infant HIV exposure (HR=1.48, 95% CI: 0.537-4.09). Maternal SARS-CoV-2 was associated with a >10-fold increased risk of infant infection (HR=10.3, 95% CI: 2.89-36.8). Twenty percent of participants had symptoms, but no participant experienced severe COVID-19 or death. Seroreversion occurred in [~]30% of mothers and infants. SARS-CoV-2 sequences obtained from stool were related to contemporaneously circulating variants. ConclusionsThese data indicate that postpartum Kenyan women and their infants were at high risk for SARS-CoV-2 infection in 2020, and that antibody responses waned rapidly. However, most cases were asymptomatic and healthy women living with HIV did not have a substantially increased risk of infection or severe COVID-19.

Emergence of a SARS-CoV-2 E484K variant of interest in Arizona

SARS-CoV-2 is locked in a high-stakes arms race between the dynamics of rising population immunity and escape mutations. The E484K mutation in the spike protein reduces neutralization by post-vaccination sera and monoclonal antibody therapeutics. We detected the emergence of an E484K harboring variant B.1.243.1 from a common circulating variant (B.1.243) in the United States. In contrast to other instances when the E484K mutation was acquired independently in the parental lineage, genomic surveillance indicates that the B.1.243.1 variant of interest is in the process of being established in Arizona and beginning to cross state borders to New Mexico and Texas. Genomic, epidemiologic and phylogenetic evidence indicates that the B.1.243.1 variant of interest is poised to emerge. These findings demonstrate the critical need to continue tracking SARS-CoV-2 in real-time to inform public health strategies, diagnostics, medical countermeasures and vaccines.

Defining the Pandemic at the State Level: Sequence-Based Epidemiology of the SARS-CoV-2 virus by the Arizona COVID-19 Genomics Union (ACGU)

In December of 2019, a novel coronavirus, SARS-CoV-2, emerged in the city of Wuhan, China causing severe morbidity and mortality. Since then, the virus has swept across the globe causing millions of confirmed infections and hundreds of thousands of deaths. To better understand the nature of the pandemic and the introduction and spread of the virus in Arizona, we sequenced viral genomes from clinical samples tested at the TGen North Clinical Laboratory, provided to us by the Arizona Department of Health Services, and at Arizona State University and the University of Arizona, collected as part of community surveillance projects. Phylogenetic analysis of 79 genomes we generated from across Arizona revealed a minimum of 9 distinct introductions throughout February and March. We show that >80% of our sequences descend from clades that were initially circulating widely in Europe but have since dominated the outbreak in the United States. In addition, we show that the first reported case of community transmission in Arizona descended from the Washington state outbreak that was discovered in late February. Notably, none of the observed transmission clusters are epidemiologically linked to the original travel-related cases in the state, suggesting successful early isolation and quarantine. Finally, we use molecular clock analyses to demonstrate a lack of identifiable, widespread cryptic transmission in Arizona prior to the middle of February 2020.

An 81 base-pair deletion in SARS-CoV-2 ORF7a identified from sentinel surveillance in Arizona (Jan-Mar 2020)

On January 26 2020, the first Coronavirus Disease 2019 (COVID-19) case was reported in Arizona of an individual with travel history (3rd case in the US) (1). Here, we report on early SARS-CoV-2 sentinel surveillance in Tempe, Arizona (USA). Genomic characterization identified an isolate encoding a 27 amino acid in-frame deletion in accessory protein ORF7a, the ortholog of SARS-CoV immune antagonist ORF7a/X4.