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We report a case of 50-year-old Japanese male who developed periungual desquamation in hand and feet, during recovery phase of severe COVID-19. As coronary lesions (CALs) have been reported during the recovery phase of severe COVID-19 in children as well as Kawasaki disease, caution may be necessary in adults as well.

The coronavirus disease 2019 (COVID-19) pandemic has caused an exponential rise in death rates and hospitalizations. The aim of this study was to characterize the D614G substitution in the severe acute respiratory syndome coronavirus 2 (SARS-CoV-2) spike glycoprotein (S protein), which may affect viral infectivity.

The effect of D614G substitution on the structure and thermodynamic stability of the S protein was analyzed with use of DynaMut and SCooP. HDOCK and PRODIGY were used to model furin protease binding to the S protein RRAR cleavage site and calculate binding affinities. Molecular dynamics simulations were used to predict the S protein apo structure, the S protein-furin complex structure, and the free binding energy of the complex.

The D614G substitution in the G clade of SARS-CoV-2 strains introduced structural mobility and decreased the thermal stability of the S protein (ΔΔG = -0.086 kcal mol

). ITF3756 in vitro The substitution resulted in stronger binding affinity (K

 = 1.6 × 10

) for furin, which may enhance S protein cleavage. The results were corroborated by molecular dynamics simulations demonstrating higher binding energy of furin and the S protein D614G mutant (-61.9 kcal mol

compared with -56.78 kcal mol

for wild-type S protein).

The D614G substitution in the G clade induced flexibility of the S protein, resulting in increased furin binding, which may enhance S protein cleavage and infiltration of host cells. Therefore, the SARS-CoV-2 D614G substitution may result in a more virulent strain.

The D614G substitution in the G clade induced flexibility of the S protein, resulting in increased furin binding, which may enhance S protein cleavage and infiltration of host cells. Therefore, the SARS-CoV-2 D614G substitution may result in a more virulent strain.

Clinicians are commonly taught that if patients with suspected rickettsial disease have continuing fever after 48 hours of anti-rickettsial therapy, an alternative diagnosis is likely.

This retrospective study of patients hospitalised with scrub typhus and Queensland tick typhus (QTT) in tropical Australia, examined the time to defervescence after initiation of the patients’ anti-rickettsial therapy. It also identified factors associated with delayed defervescence (time to defervescence >48 hours after antibiotic commencement).

Of the 58 patients, 32 (56%) had delayed defervescence. The median (interquartile range (IQR)) age of patients with delayed defervescence was 52 (37-62) versus 40 (28-53) years in those who defervesced within 48 hours (p = 0.05). Patients with delayed defervescence were more likely to require Intensive Care Unit (ICU) admission than those who defervesced within 48 hours (12/32 (38%) versus 3/26 (12%), p = 0.02). Even among patients not requiring ICU care, patients with delayed defervescence required a longer hospitalisation than that those who defervesced within 48 hours (median (IQR) 6 (3-8) versus 3 (2-5) days, p = 0.006).

A significant proportion of patients with confirmed scrub typhus and QTT will remain febrile for >48 hours after appropriate anti-rickettsial therapy. Delayed defervescence is more common in patients with severe disease.

48 hours after appropriate anti-rickettsial therapy. Delayed defervescence is more common in patients with severe disease.

Numerous of cases of chilblains have been observed, mainly in young subjects with no or mild symptoms compatible with COVID-19. The pathophysiology of these lesions is still widely debated and an association with SARS-CoV-2 infection remains unconfirmed.

This paper focus on the unresolved issues about these COVID toes and in particular whether or not they are associated with COVID-19.

The temporal link between the outbreak of chilblains and the COVID-19 pandemic is a first suggests a link between the two events. Positive anti-SARS-CoV/SARS-CoV-2 immunostaining on skin biopsy of chilblains seem to confirm the presence of the virus in the lesions, but lack specificity and must be interpreted with caution. Conversely, RT-PCR and anti-SARS-CoV-2 serology were negative in the majority of patients with chilblains. Therefore, SARS-CoV-2 infection can be excluded, with relative certainty, even after accounting for possible lower immunization in mild/asymptomatic patients and for some differences in sensitivity/ repeated testing of larger numbers of patients and the need for valid follow-up data that take into consideration epidemic curves and evolution of lockdown measures.

Understanding the proportion of pandemic deaths captured as ‘laboratory-confirmed’ deaths is crucial. We assessed the ability of laboratory-confirmed deaths to capture mortality in the EU during the 2009 pandemic, and examined the likelihood that these findings are applicable to the SARS-CoV-2 pandemic.

We present unpublished results from the Global Pandemic Mortality (GLaMOR) project, in which country-specific mortality estimates were made for the 2009 influenza H1N1p pandemic. These estimates were compared with laboratory-confirmed deaths during the 2009 pandemic to estimate the ability of surveillance systems to capture pandemic mortality.

For the 2009 influenza H1N1p pandemic, we estimated that the proportion of true pandemic deaths captured by laboratory-confirmed deaths was approximately 67%. Several differences between the two pandemics (e.g. age groups affected) make it unlikely that this capture rate will be equally high for SARS-CoV-2.

The surveillance of laboratory-confirmed deaths in the EU during the 2009 pandemic was more accurate than previously assumed. We hypothesize that this method is less reliable for SARS-CoV-2. Near-real-time excess all-cause mortality estimates, routinely compiled by EuroMOMO, probably offer a better indicator of pandemic mortality. We urge more countries to join this project and that national-level absolute mortality numbers are presented.

The surveillance of laboratory-confirmed deaths in the EU during the 2009 pandemic was more accurate than previously assumed. We hypothesize that this method is less reliable for SARS-CoV-2. Near-real-time excess all-cause mortality estimates, routinely compiled by EuroMOMO, probably offer a better indicator of pandemic mortality. We urge more countries to join this project and that national-level absolute mortality numbers are presented.