Il Covid europeo viene da un'esperimento GOF USA fuori controllo originariamente diretto CONTRO LA CINA: era l'unico asso nella manica di Trump ma SI e' rivelato la classica zappata ai propri piedi

 

Most Early New York COVID-19 Cases Came From Europe

June 4, 2020

Though most trace the coronavirus outbreak to China, a new analysis finds most of the cases in New York seem to have originated in Europe.

coronavirus, NYC, new york, covid-19

Officially, the first case of coronavirus disease 2019 (COVID-19) was reported in New York City on February 29, but a new report based on genomic analysis suggests the disease was introduced as early as January, and that most cases were linked to Europe, rather than Asia.

The report, published in the journal Science, helps paint a picture of the early days of the spread of SARS-CoV-2 in what would become the major COVID-19 hotspot in the US.

Corresponding author Harm van Bakel, PhD, of the Icahn School of Medicine at Mount Sinai, explained that the medical school has a multidisciplinary pathogen analysis program called the Pathogen Surveillance Program. When COVID-19 hit, the lab was able to use that existing infrastructure to evaluate 90 SARS-CoV-2 isolates from 84 patients who visited the health system between February 29 and March 18.

Those isolates tell a considerable amount about how the virus arrived and spread in New York, according to van Bakel and co-authors.

“Based on genetic similarity and phylogenetic analysis of full-length viral genome sequences, most cases diagnosed during the 18 days after the first-reported COVID-19 case in New York State appear to be associated with untracked transmission and potential travel-related exposure,” the authors write.

However, van Bakel and colleagues said it does not appear that most cases originated in Asia. Instead, the majority of introductions of the virus seem to have come from Europe and from elsewhere in the United States.

As for community transmission, the authors report that 21 cases of COVID-19 appeared to be closely related, which is evidence that they are the result of community spread.

In their analysis, the authors assigned each SARS-CoV-2 isolate to a main monophyletic clade based on amino acid and nucleotide substitutions and statistical information using the maximum-likelihood and Bayesian methods.

The first two isolates came from patients with recent travel to the Middle East and Europe and thus were excluded from inferences made based on phylogenetic analysis.

Of the remaining isolates, the vast majority (87%) clustered with clade A2a, and the majority of isolates in that clade (72%) are cases of patients with COVID-19 in Europe, suggesting that Europe was the major origin of COVID-19 cases in New York in march, the authors write.

The investigators say it is likely these cases began in New York between late January and mid-February. Another 6% of isolates fit in clase A1a, which is also made up largely of isolates originating in Europe.

The remaining clades (B, B1, and B4) are cases believed to have been introduced in New York between February and early March. Two of the introductions appear to have come from Washington State. A majority of the sequences in the B clade originated in Asia, though the authors report that the closest relatives of the New York isolates originated in Europe and North America.

“We find clear evidence for multiple independent introductions into the NYC metropolitan area from different regions globally, as well as from other parts of the United States,” investigators wrote.

Notably, investigators said cases that were identified based on travel histories resulted in quick quarantine and hospitalization and do not appear to be linked to significant community spread.

“We find that New York City, as an international hub, provides not only a snapshot of the diversity of disease-causing SARS-CoV-2, at the global level, but also informs on the dynamics of the pandemic at the local level,” investigators concluded.


Trends in COVID-19 Hospitalized Patients and the Impact of Remdesivir

A retrospective comparative effectiveness study looked at time to clinical improvement or time to death among hospitalized patients who were treated with or without remdesivir.

remdesivir

As hospitalizations start to creep back up in the United States, the precarious position we are in with COVID-19 response is one that underscores how effective our interventions are. Since this pandemic began, there have been nearly two million hospital admissions for COVID-19 patients. Cases are slowly climbing, with the 7-day moving average increasing per the Centers for Disease Control and Prevention (CDC). Now is the time where we race to vaccinate as many people as possible while encouraging continued vigilance with COVID-19 prevention efforts.

Treatment of patients with COVID-19 is one particular piece to response that is challenging. We’ve gotten better at it, but responding to a novel respiratory pathogen is hard enough and made worse by a pandemic lasting well over a year in a fatigued healthcare workforce. As we move towards the next phase in this pandemic with a disease that is likely going to be more endemic than entirely eliminated, the treatment of patients will become increasingly important and require precision.

new publication in JAMA Network Open sought to address some of the treatment questions for those patients hospitalized with COVID-19 and if they were treated with remdesivir. The authors performed a retrospective comparative effectiveness study looking at time to clinical improvement or time to death among hospitalized patients who were treated with or without remdesivir.

For those treated, the question was also asked if it was alone or with corticosteroids. Patients included in this retrospective review were hospitalized between March 4 to August 29, 2020 across five hospitals in Maryland and the Washington D.C. area that compromise the Johns Hopkins Medicine System. All studied patients tested positive for SARS-CoV-2/COVID-19 via RT-PCR.

Among those 2,299 studied patients, nearly 15% received remedesivir, of whom the median age was 60 and 44.7% were women. 80.7% were self-identified as non-White and the median time from admission to treatment was 1.1 days. The authors noted that in terms of time to clincal management – “Of 570 matched individuals (285 remdesivir and 285 matched controls), 236 (82.8%) patients who received remdesivir and 213 (74.7%) controls achieved clinical improvement before 28 days, with a median time to clinical improvement of 5.0 days (IQR, 4.0-8.0 days) for remdesivir recipients and 7.0 days (IQR, 4.0-10.0 days) for controls. In Cox proportional hazards regression models, remdesivir treatment was associated with significantly shortened time to clinical improvement (adjusted hazard ratio [aHR], 1.47 [95% CI, 1.22-1.79])”.

Whereas for time to death- Remdesivir recipients had a 28-day mortality rate of 7.7% (22 deaths) compared with 14.0% (40 deaths) for matched controls, but this difference was not statistically significant in the time-to-death analysis (aHR, 0.70; 95% CI, 0.38-1.28). The median time to death was 8.6 days (IQR, 6.1-14.2 days) for remdesivir recipients and 8.2 days (IQR, 4.8-13.8 days) for controls”. Adding corticosteroids to treatment with remedesivir did not appear to reduce the hazard of death within the 28-day monitoring period.

Overall, these findings point to a more speedy recovery when remdesivir was utilized in hospitalized patient, but more studies are wholly needed. More targeted interventions to not only reduce severe disease and mortality are critical, but also to help shorten the period of treatment and hospitalization, which can increase the risk for healthcare-associated infections.


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