Coronavirus: Boris Johnson has tested positive for coronavirus @BBC News – BBC

Boronavirus

80% destroy building free corona

I bet BBC is ashamed of making fun of Iranian officials getting infected.

Get well borris

Get Well Please, you're doing a fantastic job protecting UK…

Not one cough???

If Boris goes who's gonna be next?

This virus was manufactured to wipe out the human race, just like aids. All crap that it started in China. Let’s talk about Russia. Not a single word.

Get well soon Boris 🇬🇧🤜🤛🇬🇧

Hope that's takes the piss out of you mate

he aint been washing his hands enough :0

Good

A number of pre-clinical and clinical trials around use of plasma from patients who have recovered are underway, however, and there are some promising signs that convalescent plasma could indeed be effective against SARS-CoV-2.

This is hardly the first time that convalescent plasma has been proposed or attempted to fight off a disease. People who have had a virus and subsequently recovered from it typically build up an immunity to it — either long-term, as with chicken pox, or short-term, as with the seasonal flu. Logically, it stands to reason that it should be possible, at least in theory, to take the antibodies from one individual who has already developed them, and transfuse them into a patient whose immune system is not doing a good enough job producing its own.

Convalescent plasma transfusions have been used in previous outbreaks, including against the H1N1 flu, as well as the original SARS and MERS epidemics, with varying results.

A number of research projects are underway regarding use of plasma against COVID-19, that studied 10 severe patients who received donations from recently recovered patients. That study found that in five of the 10 cases, the level of antibodies “increased rapidly” immediately post-transfusion (four other patients already had a high level of antibodies, and that persisted), and that within a week, the presence of the virus was undetectable in seven patients.

That still isn’t a formal clinical study, but other small-scale investigations from clinical practice have shown similar results. A group of doctors and researchers have also put together a set of protocols for use by doctors working with both donors and recipients to help align efforts across investigations and ensure that everyone working on this problem in the medical science community is working from the same playbook.

All donor patients would have to be tested to confirm that they are not at risk of transmitting the virus. While some early studies have shown that plasma transfusions could be effective in prophylactic use (meaning treating healthy people before they encounter the virus.

As with all the treatments currently under development, this will take a lot of testing and research both to validate, and then to certify for general use — though there are a lot of researchers working on those challenges, because work to date shows this is likely to be more effective as a strategy in cases that haven’t yet progressed to the severe symptom stage. Convalescent plasma treatment isn’t new, or even all that sophisticated, but it does have the advantage of being relatively safe (in line with standard blood transfusions, once a person is confirmed to no longer be carrying any active virus), so this could be something to watch for more active updates versus some of the longer-lead treatment technologies in development.

Treatment

-we present a summary of current knowledge regarding the coronavirus not seen in the media nor given out by the gov

The current best strategy of treatment of patients with COVID-19 is purely supportive. Clinicians and intensive care specialists are applying much of what they have learned during the SARS epidemic to guide current therapy of COVID-19. Recommendations for admission to critical care units, guidelines for infection control, and procedures to minimize nosocomial transmission are being established [52]. However, there are several fronts that are being studied to develop targeted treatments.

The most efficient approach to the treatment of COVID-19 is to test whether existing antiviral drugs are effective. In previous betacoronavirus epidemics, several antiviral drugs, such as ribavirin, interferon, lopinavir-ritonavir, and darunavir/cobicistat (prezcobix) were tested, with some showing promising in vitro results [53]. Remdesivir, an adenosine analog used against RNA viruses (including SARS and MERS-CoV), was a candidate Ebola treatment with promising in vitro results but disappointing in vivo effects against Ebola [54,55]. There is currently in vitro evidence that remdesivir may be effective in controlling SARS-CoV-2 infection [56]. In fact, compassionate use of remdesivir was employed in the treatment of the first COVID-19 case in the United States, during a period of rapid clinical deterioration, and within one day there was dramatic improvement of the clinical condition [57]. Randomized double-blinded, placebo-controlled clinical trials are currently underway in China and USA to evaluate the efficacy of remdesivir and initial results are expected by the end of April 2020 [58,59].

Other existing drug candidates include chloroquine and camostat mesylate. Chloroquine is a widely used anti-malarial drug that is known to block virus-cell fusion and has been shown to interfere with the glycosylation of SARS-CoV and ACE-2 cellular receptors, rendering the ACE-2-SARS-CoV interaction less efficient [60]. There is also in vitro evidence that chloroquine may be effective in preventing SARS-CoV-2 cellular entry [56]. Camostat mesylate, also known as FOY 305 [61], was initially developed and currently approved for the treatment of chronic pancreatitis in Japan [62,63]. Camostat mesylate targets the TMPRSS2 protease, theoretically preventing viral entry. Researchers in Germany showed that camostat mesylate reduced the amount of SARS-CoV-2 viral replication [64].

A simple but very effective treatment modality is the use of convalescent plasma, or serum from patients who have recovered from the virus, to treat patients. Patients with resolved viral infection will have developed a specific antibody response which may be helpful in neutralizing viruses in newly infected individuals. This modality was successfully employed during the 2014–2015 Ebola outbreak [65,66]. However, the use of convalescent sera is of limited benefit in an outbreak situation since the exponential growth of infected patients exceeds the ability of previous patients to provide donor plasma.

The recent finding that SARS-CoV-2 binds to the same ACE-2 receptors targeted by the 2002 SARS-CoV [24] opens up the possibility of using the previous research on the 2002 SARS epidemic and applying it to COVID-19. The first strategy would be to employ either a small receptor-binding domain (RBD) or a neutralizing antibody targeting the ACE-2 receptor, thus blocking the binding of S protein and preventing virus entry into cells. Initial in vitro results have shown promising results [67,68] and specific monoclonal antibodies are being contemplated as candidates for treatment [69,70]. The main limitation of using RBDs or antibodies is that the treatment must be given within a specific time window, before the initiation of viral replication [20]. In addition, the side effects of ACE-2 blockade, especially since ACE-2 is also present in non-pulmonary tissue, must be understood and minimized before implementation. In addition, finally, the turnover of ACE-2 receptors would influence how often the therapeutic RBD or antibody would have to be administered.

A second strategy is to create an ACE-2-like molecule that would bind to the S protein of the coronavirus itself. Again, research in to the 2002 SARS virus demonstrated that soluble ACE-2 proteins blocked the SARS virus from infecting cells in vitro [68,71]. The additional benefit to using this strategy lies in the possible prevention of S protein-mediated ACE-2 shedding that has been shown to induce the pulmonary edema characteristic of SARS [72,73]. A phase II clinical trial of recombinant ACE-2 in ARDS reported significant modulation of inflammatory proteins, but no significant differences in respiratory parameters [74]. Further research is necessary to assess if the animal studies will translate to clinical benefit.

There are currently more than 80 clinical trials to test a variety of potential SARS-CoV-2 treatments [75].

7. Vaccine Development

The long-term goal of SARS-CoV-2 research is developing an effective vaccine to yield neutralizing antibodies. The National Institutes of Health in the US, and Baylor University in Waco, Texas, are working on a vaccine based on what they know about the coronavirus in general, using information from the SARS outbreak. In addition, the recent mapping of the SARS-CoV-2 spike protein may pave the way for more rapid development of a specific vaccine [76]. Of interest is the use of a relatively new vaccine technology, RNA vaccines that have the ability to elicit potent immune responses against infectious diseases and certain cancers [77,78]. Traditional vaccines stimulate the production of antibodies via challenges with purified proteins from the pathogens, or by using whole cells (live, attenuated vaccines)[email protected]@@@@@@@@@ While very effective, the creation of new vaccines can take [email protected]@@@@@@@@@ Alternatively, RNA-based vaccines use mRNA that upon entering cells, are translated to antigenic molecules that in turn, stimulate the immune system. This process has been used effectively against some cancers [79,80], and clinical trials are underway for several other cancers [81]. In addition, the production of RNA-based vaccines is more rapid and less expensive than traditional vaccines, which can be a major advantage in pandemic situations. Clinical trials for an mRNA-based SARS-CoV-2 vaccine are currently underway [82]. Study subjects will receive the mRNA vaccine in two doses, 28 days apart and the safety and immunogenicity will be assessed.

I

so how many people has he infected so far ? in addition to brexit scheme

Have you got the conviras #boris #wach out