The takeaway: Even though mutations happen in all virus, vaccines still work. Current evidence about SARS-CoV-2 indicates that an effective COVID-19 vaccine can be obtained, and that it should be able to provide immunity against the virus.

The claim: A better analogy for COVID-19 is the mumps. For more than 45 years, we’ve had a very effective vaccine for measles, mumps, and rubella (which are also RNA viruses).

The evidence: We are all imperfect and we all make mistakes. For a virus, a mistake means the introduction of a mutation in its sequence, and RNA viruses (like the flu, mumps, measles virus, and SARS-CoV-2) have the highest error rates in nature. Mutations are indispensable for viral survival and evolution; this property is believed to benefit the viral population, allowing it to adapt and respond to different complex environments encountered during spread between hosts, within organs and tissues, and in response to the pressure of the host immune response [1]. How fast a virus is changing can be estimated by measuring its mutation rate, and then they can be classified as changing fast – high mutation rate – like HIV or Influenza, or as stable, like measles or mumps virus. SARS-CoV-2 has a mutation rate three times slower than the flu virus [2], but it's still changing faster than the mumps virus (the mutation rate of influenza is more than 10 times higher than mumps) [3]. Of course, how fast a virus can change has implications in the efficacy of treatments and vaccines, but it's not the only determinant. Even though mutations happen in all viruses, vaccines still work. A great example is the measles virus, as the antigenic composition of the vaccine (the molecules that “wake up” the immune system) used to prevent it has remained efficient since it was developed, in the 1960s, and confers protection against the 24 circulating genotypes [4]. The same is true for the mumps virus, with a vaccine that has been efficient for many decades [5]. Sequencing data suggest that coronaviruses change more slowly than most other RNA viruses, probably because of a viral ‘proofreading’ activity that corrects all the copying mistakes [6]. Taken together, all this evidence indicates that an effective COVID-19 vaccine can be obtained, and that it should be able to provide lasting immunity against the virus.

Sources:<br> 1

2 SARS-CoV-2 mutation rate: 1.26 x 10-3 substitutions/site/year

3 Influenza (flu-virus) mutation rate: 3.68 x 10-3 substitutions/site/year. Mumps mutation rate: 2.98 × 10−4 substitutions/site/year

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Take away: Even though mini-lungs (and mini-organs) are extremely valuable tools for scientist to study disease and prospective therapeutics, results obtained with these models are hardly generalizable and normally need to be validated in animal models and clinical studies.

The claim: Based on our model we can tackle many unanswered key questions, such as understanding genetic susceptibility to SARS-CoV-2, assessing relative infectivity of viral mutants, and revealing the damage processes of the virus in human alveolar cells. Most importantly, it provides the opportunity to develop and screen potential therapeutic agents against SARS-CoV-2 infection.

The evidence: Regardless of their name, mini-organs are hardly real miniature organs, these clumps of cells resemble organs in many ways, but they lack certain features that allow real organs to function and grow. For now, mini-organs don’t develop beyond tiny and simplistic models of organs, and remain hard to produce in the large, consistent batches needed for drug screening and other efforts. But, in spite of their limitations, they still are a giant step up from 2D cultures of cells that scientists have long grown in the lab. In particular, studies of SARS-CoV-2 in mini-organs have limitations because they do not reflect the crosstalk between organs and systems that happens in the body. Here for example, the mini-organs do not produce the full cellular spectrum present in the adult alveoli. Also, the mini-lungs in this study cannot mimic an interaction with the immune system, which likely influences how the disease develops. Some groups are beginning to test existing drugs against SARS-CoV-2 in mini-organs in a small scale, but we will only know at the end of this process what the predictive value of these systems are for testing drug efficacy.

Source: https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(20)30498-7 https://www.nature.com/articles/ncb3312 https://www.biorxiv.org/content/10.1101/2020.06.10.144816v1 https://www.biorxiv.org/content/10.1101/2020.05.25.115600v2