RESUMO
BACKGROUND: SARS-CoV-2 is the virus responsible for the current global pandemic, COVID-19. Because this virus is novel, little is known about its sensitivity to disinfection. METHODS: We performed suspension tests against SARS-CoV-2 using three commercially available quaternary ammonium compound (Quat) disinfectants and one laboratory-made 0.2% benzalkonium chloride solution. FINDINGS: Three of the four formulations completely inactivated the virus within 15 s of contact, even in the presence of a soil load or when diluted in hard water. CONCLUSION: Quats rapidly inactivate SARS-CoV-2, making them potentially useful for controlling SARS-CoV-2 spread in hospitals and the community.
Assuntos
Compostos de Benzalcônio/farmacologia , COVID-19/prevenção & controle , Higienizadores de Mão/farmacologia , Compostos de Amônio Quaternário/farmacologia , SARS-CoV-2/efeitos dos fármacos , Anti-Infecciosos Locais/química , Anti-Infecciosos Locais/farmacologia , Compostos de Benzalcônio/química , COVID-19/diagnóstico , COVID-19/epidemiologia , COVID-19/virologia , Desinfetantes/química , Desinfetantes/classificação , Desinfetantes/farmacologia , Desinfecção/métodos , Higienizadores de Mão/química , Humanos , Compostos de Amônio Quaternário/química , SARS-CoV-2/genética , SARS-CoV-2/crescimento & desenvolvimento , Resultado do TratamentoRESUMO
Previous gene transfer studies of the herpes simplex virus type 1 (HSV-1) using the latency-associated transcript (LAT) promoter have reported a decrease in transgene expression in the brain over time, but the extent of this decrease has not been measured and it is unknown if expression eventually stabilizes. We examined LAT promoter-mediated transgene expression in the mouse brain for 1 year following intracranial injection with a HSV-1 vector expressing human beta-glucuronidase (GUSB). The vector genome copy number remained stable from 2 to 52 weeks. Quantitative reverse transcriptase PCR detected a peak of LAT intron expression at 2 weeks (corresponding to the end of the acute phase of viral infection), followed by stable expression during latency (13-52 weeks). The number of GUSB-positive cells also had a peak in the acute phase and then was stable during latency (13-52 weeks). GUSB enzymatic activity was maintained at 11% of normal at 6 and 12 months, indicating that the LAT promoter is capable of driving stable transgene expression in the brain.