Detection of co-infection and recombination cases with Omicron and local Delta variants of SARS-CoV-2 in Vietnam

The first nationwide outbreak of COVID-19 in Vietnam started in late April 2021 and was caused almost exclusively by a single Delta lineage, AY.57. In early 2022, multiple Omicron variants co-circulated with Delta variants and quickly became dominant. The co-circulation of Delta and Omicron happened leading to possibility of co-infection and recombination events which can be revealed by viral genomic data. From January to October 2022, a total of 1028 viral RNA samples out of 4852 positive samples (Ct < 30) were sequenced by the long pooled amplicons method on Illumina platforms. All sequencing data was analysed by the workflow for SARS-CoV-2 on CLC genomics workbench and Illumina Dragen Covid application. Among those sequenced samples, we detected a case of Delta AY.57/Omicron BA.1 co-infection and two cases of infection with Delta AY.57/Omicron BA.2 recombinants which were nearly identical and had different epidemiological characteristics. Since the AY.57 lineage circulated almost exclusively in Vietnam, these results strongly suggest domestic events of co-infection and recombination. These findings highlight the strengths of genomic surveillance in monitoring the circulating variants in the community enabling rapid identification of viral changes that may affect viral properties and evolutionary events

Spatiotemporal evolution of SARS-CoV-2 Alpha and Delta variants during large nationwide outbreak of COVID-19, Vietnam, 2021

We analyzed 1,303 SARS-CoV-2 whole-genome sequences from Vietnam, and found the Alpha and Delta variants were responsible for a large nationwide outbreak of COVID-19 in 2021. The Delta variant was confined to the AY.57 lineage and caused >1.7 million infections and >32,000 deaths. Viral transmission was strongly affected by nonpharmaceutical interventions

COVID-19 patients hospitalized after the fourth wave of the pandemic period in Vietnam: Clinical, laboratory, therapeutic features, and clinical outcomes

Background/Purpose: Despite having relatively high COVID-19 vaccine coverage in Vietnam, a fraction of COVID-19 patients required hospitalization due to severe symptoms. The purpose of this study was to describe the clinical, laboratory, complications, and treatment of COVID-19 patients hospitalized during the pandemic's fourth wave. Methods: Genome sequencing was performed on COVID-19 patients. Data on clinical characteristics, treatment, complications, and outcomes were consistently collected. Results: The clinical classifications were mild (37.43%), moderate (24.2%), and severe (38.37%). Patients with co-morbidities, high fever >39 °C, hypertension, tachycardia, tachypnea, and SpO2<90%, had a 1.2–4 folds higher of severe progression than those with mild/moderate. Serious consequences were much more common in the severe patients than in the mild/moderate. The respiratory system of severe patients was generally documented as fine, coarse crackles, and CT scanner shown ground glass, consolidation, and opacity, with Delta variant accounting for 92.6%. Complications were common in the severe patients, including bacteria pneumonia (36.42%), ARDS (61.11%), blood clotting disorder (7.14%), infection (46.92%), and acute kidney injury (12.35%). Antiviral, antifungal, corticosteroid, anticoagulant, and ECMO regimens were utilized. Patients died mostly as a result of co-morbidities, low SpO2, lung injury, and complications such as bacterial + fungal pneumonia (83.9%), ARDS (83.9%), bacteremia (56.5%), injury acute renal failure (27.4%), and coagulopathy (12.9%). Conclusion: Severe and critical COVID-19 patients frequently have several comorbidities, multiple lung lesions along with a variety of clinical signs. Despite receiving antivirals, antibiotics, corticosteroids, anticoagulants, and even ECMO therapy, the patient encountered multiple complications, with a fatality rate of up to 38.27%

The Mycobacterium tuberculosis cytochromes P450: Physiology, biochemistry &amp; molecular intervention

The human pathogen Mycobacterium tuberculosis (Mtb) encodes 20 cytochrome P450 (P450) enzymes. Gene essentiality for viability or host infection was demonstrated for Mtb P450s CYP128, CYP121 and CYP125. Structure/function studies on Mtb P450s revealed key roles contributing to bacterial virulence and persistence in the host. Various azole-class drugs bind with high affinity to the Mtb P450 heme and are potent Mtb antibiotics. This paper reviews the current understanding of the biochemistry of Mtb P450s, their interactions with azoles and their potential as novel Mtb drug targets. Mtb multidrug resistance is widespread and novel therapeutics are desperately needed. Simultaneous drug targeting of several Mtb P450s crucial to bacterial viability/persistence could offer a new route to effective antibiotics and minimize the development of drug resistance. </jats:p