Background The full impact of COVID‐19 on pregnancy remains uncharacterized. Current literature suggests minimal maternal, fetal, and neonatal morbidity and mortality. 1 COVID‐19 manifestations appear similar between pregnant and non‐pregnant women. 2 Objectives/Study Design We present a case of placental SARS‐CoV‐2 virus in a woman with mild COVID‐19 disease, then review the literature. RT‐PCR was performed to detect SARS‐CoV‐2. Immunohistochemistry staining was performed with specific monoclonal antibodies to detect SARS‐CoV‐2 antigen or to identify trophoblasts. Results A 29 year‐old multigravida presented at 40‐4/7 weeks for labor induction. With myalgias two days prior, she tested positive for SARS‐CoV‐2. We demonstrate maternal vascular malperfusion, with no fetal vascular malperfusion, as well as SARS‐CoV‐2 virus in chorionic villi endothelial cells, and also rarely in trophoblasts. Conclusions To our knowledge, this is the first report of placental SARS‐CoV‐2 despite mild COVID‐19 disease (no symptoms of COVID‐19 aside from myalgias); patient had no fever, cough, or shortness of breath, but only myalgias and sick contacts. Despite her mild COVID‐19 disease in pregnancy, we demonstrate placental vasculopathy and presence of SARS‐CoV‐2 virus across the placenta. Evidence of placental COVID‐19 raises concern for placental vasculopathy (potentially leading to fetal growth restriction and other pregnancy complications) and possible vertical transmission – especially for pregnant women who may be exposed to COVID‐19 in early pregnancy. This raises important questions of whether future pregnancy guidance should include stricter pandemic precautions, such as screening for a wider array of COVID‐19 symptoms, increased antenatal surveillance, and possibly routine COVID‐19 testing throughout pregnancy. This article is protected by copyright. All rights reserved.

An outbreak of respiratory disease caused by the equine-origin influenza A(H3N8) virus was first detected in dogs in 2004 and since then has been enzootic among dogs. Currently, the molecular mechanisms underlying host adaption of this virus from horses to dogs is unknown. Here, we have applied quantitative binding, growth kinetics, and immunofluorescence analyses to elucidate these mechanisms. Our findings suggest that a substitution of W222L in the hemagglutinin of the equine-origin A(H3N8) virus facilitated its host adaption to dogs. This mutation increased binding avidity of the virus specifically to receptor glycans with -glycolylneuraminic acid (Neu5Gc) and sialyl Lewis X (SLe) motifs. We have demonstrated these motifs are abundantly located in the submucosal glands of dog trachea. Our findings also suggest that in addition to the type of glycosidic linkage (e.g., α2,3-linkage or α2,6-linkage), the type of sialic acid (Neu5Gc or 5--acetyl neuraminic acid) and the glycan substructure (e.g., SLe) also play an important role in host tropism of influenza A viruses. Influenza A viruses (IAVs) cause a significant burden on human and animal health, and mechanisms for interspecies transmission of IAVs are far from being understood. Findings from this study suggest that an equine-origin A(H3N8) IAV with mutation W222L at its hemagglutinin increased binding to canine-specific receptors with sialyl Lewis X and Neu5Gc motifs and, thereby, may have facilitated viral adaption from horses to dogs. These findings suggest that in addition to the glycosidic linkage (e.g., α2,3-linked and α2,6-linked), the substructure in the receptor saccharides (e.g., sialyl Lewis X and Neu5Gc) could present an interspecies transmission barrier for IAVs and drive viral mutations to overcome such barriers.

The host tropism expansion of SARS-CoV-2 raises concern for the potential risk of reverse-zoonotic transmission of emerging variants into rodent species, including wild rat species. In this study, we present both genetic and serological evidence for SARS-CoV-2 exposure to the New York City wild rat population, and these viruses may be linked to the viruses that were circulating during the early stages of the pandemic.

SARS-CoV-2 has a higher infection rate in pregnant women than age-matched adults. With increased infectivity and transmissibility, the Delta variant is predominant worldwide. Here, we describe intrauterine fetal demise in an unvaccinated women with mild symptoms of SARS-CoV-2 Delta variant infection. Histology and elevated proinflammatory responses of the placenta suggest that fetal demise was associated with placental malperfusion due to Delta variant infection. This study suggests that the Delta variant can cause severe morbidity and mortality to fetuses. Vaccination should continve to be advocated and will likely continue to reduce SARS-CoV-2 infection risks for pregnant women and their fetuses.

Subtype H6 influenza A viruses (IAVs) are commonly detected in wild birds and domestic poultry and can infect humans. In 2010, a H6N6 virus emerged in southern China, and since then, it has caused sporadic infections among swine. We show that this virus binds to α2,6-linked and α2,3-linked sialic acids. Mutations at residues 222 (alanine to valine) and 228 (glycine to serine) of the virus hemagglutinin (HA) affected its receptor-binding properties. Experiments showed that the virus has limited transmissibility between ferrets through direct contact or through inhalation of infectious aerosolized droplets. The internal genes of the influenza A(H1N1)pdm09 virus, which is prevalent in swine worldwide, increases the replication efficiency of H6N6 IAV in the lower respiratory tract of ferrets but not its transmissibility between ferrets. These findings suggest H6N6 swine IAV (SIV) currently poses a moderate risk to public health, but its evolution and spread should be closely monitored.