Coronaviruses are enveloped positive-sensed, single-stranded RNA viruses.

ЅARЅ-СoV-2 is a betacoronavirus. It is in the same subgenus as, but is in a different clade from, the severe acute respiratory syndrome (ЅARЅ) virus

The Middle East Respiratory Syndrome (MERS) virus is a more distantly related betacoronavirus [ 7,8].

The closest RNA sequence similarities to ЅARЅ-CoV-2 are found in coronaviruses isolated from bats, which were the likely animal reservoir prior to spillover to humans [ 9,10]. Pangolins are a possible intermediate host for ЅΑRЅ-СoV-2 prior to passage to humans.

The primary host cell entry receptor for ЅΑRЅ-CоV-2 is the same as for SARS-CoV, the angiotensin-converting enzyme 2 (ACE2) [11]. ЅΑRS-СоV-2 binds to ACE2 through the receptor-binding domain of its spike protein (figure 1).

Additional enzymatic interactions between ЅΑRS-CoV-2 and host cells determine specific cell tropism, which has evolved with the virus. Specifically, following ACE2 binding, the original ЅARЅ-СoV-2 virus and some subsequent variants, including Delta, enter cells after a host protease (most often the TMPRSS2 enzyme) cleaves the spike protein, enabling subsequent membrane fusion and cell entry [12,13]. Since TMPRSS2 is expressed at high levels in lung epithelial cells, these variants replicated efficiently in the lungs. Omicron-lineage variants, in contrast, mostly enter host cells through a different pathway involving cathepsin-dependent endocytosis and use the TMPRSS2-mediated pathway far less efficiently [14]. Thus, Omicron-lineage variants replicate more efficiently in the upper airways, where TMPRSS2 expression is lower than in the lungs [15].

ЅΑRS-CoV-2 antivirals have targeted one of two important viral proteins:

● RNA-dependent RNA polymerase (RdRp) – This is an error-prone enzyme responsible for viral replication [16]. Remdesivir, molnupiravir, and mindeudesivir (a drug available in Сhiոa) target the RdRp.

● 3CL protease – This is also called the main protease, and it cleaves the polyproteins encoded by the ЅΑRЅ-СоV-2 RNA. Ritonavir-boosted nirmatrelvir [17], ritonavir-boosted simnotrelvir, and ensitrelvir target this protease.

ЅΑRS-CoV-2, like many other RNA viruses, has evolved over time through random mutations from replication infidelity, although its intrinsic mutation rate is lower than many other RNA viruses (including HIV and HCV) because of a proofreading mechanism [18].

Recombination is another mechanism for evolution. This occurs when a host is simultaneously infected with two distinct ЅARЅ-СоV-2 viruses, and a progeny virus emerges that includes RNA sequences from both [19].

Rapid accumulation of many mutations may occur in highly immunocompromised individuals with persistent or chronic ЅARЅ-СoV-2 infections [18,20,21]. (See 'Viral shedding and period of infectiousness' below.)

Most importantly, selective advantage to a progeny virus mainly comes from intrinsic viral factors (often leading to replication advantage) or from greater evasion of the host immune response (most commonly from antigenic shift)

To summarize, our contributions are the following:

(i) ...

(ii) we provide an empirical comparison of prediction performance on real-world e-commerce data;

Install all the packages that you need in the new environment at the same time. Installing packages one at a time can lead to dependency conflicts.

Data scientists are also expected to be familiar with additional realms of competency. From mid-level DE skills (you have to get your data for your data science from somewhere, right?), software development skills, project management skills, visualization skills, and presentation skills

Women who did develop cancer are much more likely to be included in the study than women who did not develop cancer. Therefore, our causal graph will include a note for selection-- C-- an arrow from the outcome Y to C, and a box around C to indicate that the analysis is conditional on having been selected into the study, which means that we are only one arrow away from selection bias.