Transmission of SARS-CoV-2 Omicron Variant under a Dynamic Clearance Strategy in Shandong, China.

SARS-CoV-2 Omicron caused a large wave of COVID-19 cases in China in spring 2022. Shandong was one of the most affected regions during this epidemic yet was also among those areas that were able to quickly contain the transmission. We aimed to investigate the origin, genetic diversity, and transmission patterns of the Omicron epidemic in Shandong under a dynamic clearance strategy. We generated 1,149 Omicron sequences, performed phylogenetic analysis, and interpreted results in the context of available epidemiological information. We observed that there were multiple introductions of distinct Omicron sublineages into Shandong from foreign countries and other regions in China, while a small number of introductions led to majority of local cases. We found evidence suggesting that some local clusters were potentially associated with foreign imported cases. Superspreading events and cryptic transmissions contributed to the rapid spread of this epidemic. We identified a BA.1.1 genome with the R493Q reversion mutation in the spike receptor binding domain, potentially associated with an escape from vaccine and Omicron infection elicited neutralizing immunity. Our findings illustrated how the dynamic clearance strategy constrained this epidemic's size, duration, and geographical distribution. IMPORTANCE Starting in March 2022, the Omicron epidemic caused a large wave of COVID-19 cases in China. Shandong was one of the most affected regions during this epidemic but was also among those areas that were able to quickly contain the transmission. We investigated the origin, genetic diversity, and transmission patterns of Omicron epidemic in Shandong under a dynamic clearance strategy. We found that there were multiple introductions of distinct Omicron sublineages into Shandong from foreign countries and other regions in China, while a small number of introductions led to most local cases. We found evidence suggesting that some local clusters were associated with foreign imported cases. Superspreading events and cryptic transmissions contributed to the rapid spread of this epidemic. Our study illustrated the transmission patterns of Omicron epidemic in Shandong and provided a looking glass onto this epidemic in China.

Severe fever with thrombocytopenia syndrome virus replicates in brain tissues and damages neurons in newborn mice.

Severe fever with thrombocytopenia syndrome (SFTS) virus (SFTSV) is an emerging tick-borne phlebovirus with a high fatality rate of 12-30%, which has an expanding endemic and caused thousands of infections every year. Central nervous system (CNS) manifestations are an important risk factor of SFTS outcome death. Further understanding of the process of how SFTSV invades the brain is critical for developing effective anti-SFTS encephalitis therapeutics. We obeserved changes of viral load in the brain at different time points after intraperitoneal infection of SFTSV in newborn C57/BL6 mice. The virus invaded the brain at 3 h post-infection (hpi). Notably, the viral load increased exponentially after 24 hpi. In addition, it was found that in addition to macrophages, SFTSV infected neurons and replicated in the brain. These findings provide insights into the CNS manifestations of severe SFTS, which may lead to drug development and encephalitis therapeutics.

Study of the temperature sensitivity of severe fever with thrombocytopenia syndrome virus

This study investigated the temperature sensitivity of severe fever with thrombocytopenia syndrome virus (SFTSV) to provide a basis for SFTSV disinfection and laboratory biosafety protection. We divided SFTSV cell culture supernatants into 250 L PCR vials at 100 L/tube, and placed them in a refrigerator at 4..C, and a metal bath at 25..C, 37..C, 39..C, 56..C, and 70..C. After treatment for predetermined periods of time, the viral titer was determined through indirect immunofluorescence in Vero cells. With increasing temperature, the rate of decline of the viral titer increased. After incubation at 4..C, 25..C, 37..C, and 39..C for 24 h, the titers decreased from 107.25/100 L to 107.00/100 L, 106.75/100 L, 106.50/100 L, and 105.00/100 L, respectively. At the same temperature, with prolonged storage time, the decrease in titer became more pronounced. After SFTSV was placed at 4..C, 25..C, 37..C for 72 h, the viral titer decreased from 107.25/100 L to 106.63/100 L, 106.50/100 L, and 103.38/100 L, respectively. SFTSV lost its infectivity after incubation at 39..C for 72 h. SFTSV was inactivated after exposure to 56..C for 180 min or 70..C for 5 min. We concluded that SFTSV is inactivated after incubation at 70..C for 5 min. However, after 3 days of exposure to 4..C and 25..C, the viral titer did not change significantly. Laboratories and medical staff should focus on personal protection and disinfection of items contaminated by SFTSV.