Covid-19 / SARS-Cov2 - naučne/medicinske informacije i analize

[Asterion]

Quote

 

https://www.nytimes.com/2020/07/14/health/coronavirus-pregnancy-covid-19.html

A baby born in a Paris hospital in March to a mother with Covid-19 tested positive for the virus and developed symptoms of inflammation in his brain, said Dr. Daniele De Luca, who led the research team and is chief of the division of pediatrics and neonatal critical care at Paris-Saclay University Hospitals. The baby, now more than 3 months old, recovered without treatment and is “very much improved, almost clinically normal,” Dr. De Luca said, adding that the mother, who needed oxygen during the delivery, is healthy.

Dr. De Luca said the virus appeared to have been transmitted through the placenta of the 23-year-old mother.

 

[Asterion]

INFECTION WITH SARS-COV-2 IN ANIMALS, last update 3/7/2020

[Asterion]

Ako se kome ne spava...

 

 

Vulnerability of the industrialized microbiota

[djole]

Antitela, imunitet, mogućnost prenošenja virusa. Kako su ova tri povezana?

 

Ukoliko imate antitela, kolika je šansa da posedujete i imunitet? Ukoliko imate imunitet, kolika je šansa da i dalje budete prenosilac virusa i da zarazite druge?

 

Pošto o ovom koronavirusu ne znamo mnogo, pitanje se odnosi pre svega generalno na viruse, ili grupe virusa za koje se mogu uočiti neke pravilnosti. Što se tiče covid-19 konkretno, koliko vidim, bukvalno se trenutno ništa ne zna o ovome. Zato me interesuje kakva je situacija po ovom pitanju sa drugim virusima.

[Jataganac]

@djole mogu da ti dam laicki odgovor, ali posto je ovo naucna tema, prepusticu odgovor onima koji su dublje u materiji.

Ja jesam zavrsio srednju medicinsku, ali fizioterapija nema mnogo veze sa virusima 🙂

 

Inace, Lancet ce verovatno sutra objaviti najnovije rezultate ispitivanja vakcine koju spremaju Oksford i Astra Zeneka.

[Asterion]

On 7/16/2020 at 4:39 PM, djole said:

1.1.Antitela, imunitet, mogućnost prenošenja virusa. Kako su ova tri povezana?

 

1.2.Ukoliko imate antitela, kolika je šansa da posedujete i imunitet? Ukoliko imate imunitet, kolika je šansa da i dalje budete prenosilac virusa i da zarazite druge?

 

1.3.Pošto o ovom koronavirusu ne znamo mnogo, pitanje se odnosi pre svega generalno na viruse, ili grupe virusa za koje se mogu uočiti neke pravilnosti. Što se tiče covid-19 konkretno, koliko vidim, bukvalno se trenutno ništa ne zna o ovome. Zato me interesuje kakva je situacija po ovom pitanju sa drugim virusima.

 

1.1.Antitela su dijo imuniteta (eng. adaptive immunity) se vežu na virus i spreče, da virus ulazi u čeliju i da se dalje množi. Tako se virus ne može više širiti u telu i na drugu osobu.

Nije to jedini mehanizam preko kojeg antitela blokiraju virus.

 

1.2. Ne znam to o šansam...odgovoriču ti ovako...imaš protitela protvi nekog virusa i još uvek imaš virus u telu i možeš ga raznositi. Zove se latencija odnosno Latency. Više u spoileru.

 

Latency

Inapparent infections (those that do not cause specific signs and symptoms) often result after exposure to picornaviruses, influenza viruses, rhinoviruses, herpesviruses, and adenoviruses but less frequently to measles and chickenpox viruses. In cases of inapparent infection, long-lasting immunity develops, but only to the strain of virus that has the same antigenic composition as the original infecting virus.

Certain of these viruses persist in the tissues of the host after the initial infection despite the presence of circulating antibodies to it in the blood and tissues. Such viruses probably reside inside cells, where they are protected from antibodies that cannot penetrate the cell membrane. Among persistent viruses are adenoviruses, measles virus, and, in particular, many kinds of herpesviruses. The genetic information of herpesviruses and adenoviruses can be integrated into the genome of the host cell, but it is believed that these viruses frequently, and the measles virus invariably, reside in cells in the form of extrachromosomal genes (genes not integrated in chromosomes). These dormant viruses can be activated by many factors, such as trauma, another infection, emotional stress, menstruation, excessive exposure to sunlight, and various illnesses.

The phenomenon of latency and reactivation is particularly common among viruses of the family Herpesviridae, which cause chronic or recurrent diseases: (1) herpes simplex virus type 1, which causes recurrent cold sores, (2) herpes simplex virus type 2 in genital tissue, which causes repeated herpetic infections of the vagina or penis, (3) cytomegalovirus, which usually produces an inapparent infection activated by simultaneously occurring disease to cause severe liver, lung, or nervous-system disease, and (4) varicella virus, which is the causative agent of chickenpox but which can be activated decades later to produce herpes zoster (shingles). A rare, but invariably fatal, disease of the nervous system is subacute sclerosing panencephalitis (SSPE), which is a progressive degenerative condition caused by measles virus (a paramyxovirus) lying dormant in brain cells for many years and then reactivated, usually in adolescence. There is no simple explanation for why latent viruses, such as those in the family Herpesviridae, that are present in the tissues of most adult humans can be activated to cause disease in some people but not in others.

 

Chronic and slowly progressive diseases

Although some viruses multiply slowly, this is not always the explanation for the chronicity or the slow progression of the diseases caused by these viruses. Hepatitis, for example, is a subacute or chronic disease, with a long latent period, that is caused by at least five viruses with different properties. Hepatitis A is caused by a picornavirus usually transmitted by the fecal-oral route in a manner similar to that of poliovirus. Hepatitis B is caused by a small DNA virus that contains its own DNA polymerase and is transmitted by transfusion of blood and other blood products, by the sharing of nonsterile hypodermic needles among drug users, by sexual intercourse, or from mother to neonate. Hepatitis B virus is classified with similar viruses of birds in the family Hepadnaviridae. Most cases of hepatitis spread by the transfusion of blood or blood products or by needles shared by drug users are caused by a third, completely distinct virus—originally called non-A, non-B hepatitis but now known to be a member of the virus family Flaviviridae—designated hepatitis C virus. A fourth unique agent that causes hepatitis is designated hepatitis delta virus, which has not yet been classified taxonomically but is a small enveloped virus containing a circular RNA genome; hepatitis B virus serves as a helper for replication of hepatitis delta virus, the virions of which contain hepatitis B surface antigen (HB_sAg). The fifth causative agent of viral hepatitis, largely occurring in Asia and Africa, is a small RNA virus tentatively classified as a member of the family Caliciviridae and designated hepatitis E virus.

Many other agents that appear to cause chronic and slowly progressive diseases, particularly those affecting the nervous system, have been identified. A fatal neurological disorder of sheep, called scrapie, has an incubation period of years and may be caused by a heat-resistant protein called a prion, which is self-replicating. Similar, rather obscure agents have been identified for two uncommon fatal disorders of the nervous system called Creutzfeldt-Jakob disease and kuru.

The disease now known as AIDS was first recognized in homosexuals and hemophiliacs about 1981 and continues to be disseminated throughout the world to become one of the most devastating epidemics of all time. AIDS is caused by HIV, a member of a genetically more complex group of the family Retroviridae called lentiviruses. Closely related viruses of monkeys and cats cause similar diseases. HIV is transmitted by blood and other body fluids and infects primarily helper T lymphocytes and other cells with CD4 surface receptors (cell surface proteins that react with antigens), to which the virus binds. After the virus has been dormant for years, destruction of T lymphocytes results in drastic depression of the immune system. Death almost invariably results from “opportunistic” infections such as pneumonia—caused by ordinarily nonpathogenic organisms such as Pneumocystis carinii—or tuberculosis or by cancers such as Kaposi sarcoma and lymphomas.

 

 

 

Prevention

The spread of many viral diseases can be prevented by hygienic factors such as efficient sanitation facilities, effective waste disposal, clean water, and personal cleanliness. Active immunization by vaccines (antigen-containing preparations that elicit the synthesis of antibodies and thus immunity) has been useful in preventing common epidemics caused by acutely infectious viruses.

izvor

 

1.3.1. Još jedan tekst iz ove knjige o imunosti i virusima (generally speaking).

 

IMMUNITY TO VIRUSES

Viruses are obligatory intracellular microorganisms that use components of the nucleic acid and protein synthetic machinery of the host to replicate.

 

Viruses typically infect various cell types by receptor-mediated endocytosis after binding to normal cell surface molecules. Viruses can cause tissue injury and disease by any of several mechanisms. Viral replication interferes with normal cellular protein synthesis and function and leads to injury and ultimately death of the infected cell. This result is one type of cytopathic effect of viruses, and the infection is said to be lytic because the infected cell is lysed. Viruses can stimulate inflammatory responses that cause damage to tissues. Viruses may also cause latent infections, discussed later.

 

 



Innate and adaptive immune responses to viruses are aimed at blocking infection and eliminating infected cells (Fig. 16.8).

 

 

Innate Immunity to Viruses

The principal mechanisms of innate immunity against viruses are inhibition of infection by type I interferons and NK cell–mediated killing of infected cells. Infection by many viruses is associated with production of type I interferons (IFNs) by infected cells, and by dendritic cells, especially of the plasmacytoid type, responding to viral products (see Chapter 4). Several biochemical pathways trigger IFN production. These include recognition of viral RNA and DNA by endosomal TLRs and activation of cytoplasmic RIG-like receptors and the STING pathwayby viral RNA and DNA, respectively. These pathways converge on the activation of protein kinases, which in turn activate the IRF transcription factors that stimulate IFN gene transcription. Type I IFNs function to inhibit viral replication in both infected and uninfected cells. The mechanisms by which these cytokines block viral replication were discussed in Chapter 4 (see Fig. 4.18). NK cells kill virus-infected cells and are an important mechanism of immunity against viruses early in the course of infection, before adaptive immune responses have developed. Class I MHC expression is often shut off in virus-infected cells as an escape mechanism from CTLs. This enables NK cells to kill the infected cells because the absence of class I releases NK cells from a normal state of inhibition (see Fig. 4.10). Viral infection may also stimulate expression of activating NK cell ligands on the infected cells.

 

Adaptive Immunity to Viruses

 

Adaptive immunity against viral infections is mediated by antibodies, which block virus binding and entry into host cells, and by CTLs, which eliminate the infection by killing infected cells (see Fig. 16.8). The most effective antibodies are high-affinity antibodies produced in T-dependent germinal center reactions (see Chapter 12). Antibodies are effective against viruses only during the extracellular stage of the lives of these microbes. Viruses will be extracellular before they infect host cells, or when they are released from infected cells by virus budding or if the infected cells die. Antiviral antibodies bind to viral envelope or capsid antigens and function mainly as neutralizing antibodies to prevent virus attachment and entry into host cells. Thus, antibodies prevent both initial infection and cell-to-cell spread. Secreted antibodies, especially of the IgA isotype, are important for neutralizing viruses within the respiratory and intestinal tracts. Oral immunization against poliovirus works by inducing mucosal immunity. In addition to neutralization, antibodies may opsonize viral particles and promote their clearance by phagocytes. Complement activation may also participate in antibody-mediated viral immunity, mainly by promoting phagocytosis and possibly by direct lysis of viruses with lipid envelopes. The importance of humoral immunity in defense against viral infections is supported by the observation that resistance to a particular virus, induced by either infection or vaccination, is often specific for the serologic (antibody-defined) type of the virus. An example is influenza virus, in which exposure to one serologic type does not confer resistance to other serotypes of the virus. Neutralizing antibodies block viral infection of cells and spread of viruses from cell to cell, but after the viruses enter cells and begin to replicate intracellularly, they are inaccessible to antibodies. Therefore, humoral immunity induced by previous infection or vaccination is able to protect individuals from viral infection but cannot by itself eradicate established infection.

 

 Elimination of viruses that reside within cells is mediated by CTLs (cytotoxic T lymphocytes), which kill the infected cells. As we have mentioned in previous chapters, the principal physiologic function of CTLs is surveillance against viral infection.

 

Most virus-specific CTLs are CD8+ T cells that recognize cytosolic, usually endogenously synthesized, viral peptides presented by class I MHC molecules. If the infected cell is a tissue cell and not an antigen-presenting cell (APC), such as a dendritic cell, the infected cell may be phagocytosed by the dendritic cell, which processes the viral antigens and presents them to naive CD8+ T cells. We described this process of cross-presentation, or crosspriming, in Chapter 6 (see Fig. 6.17). Full differentiation of CD8+ CTLs often requires cytokines produced by CD4+ helper cells or costimulators expressed on infected cells (see Chapter 11). As discussed in Chapters 9 and 11, CD8+ T cells undergo massive proliferation during viral infection, and most of the proliferating cells are specific for a few viral peptides. Some of the activated T cells differentiate into effector CTLs, which can kill any infected nucleated cell. The antiviral effects of CTLs are mainly due to killing of infected cells, but other mechanisms include activation of nucleases within infected cells that degrade viral genomes and secretion of cytokines, such as IFN-γ, which activates phagocytes and may have some antiviral activity. Many lines of experimental and clinical evidence support the importance of CTLs in defense against viral infection. Susceptibility to such infections is increased in patients and animals deficient in T lymphocytes. Experimentally, mice can be protected against some virus infections by adoptive transfer of virus-specific, class I-restricted CTLs. Viruses have developed numerous strategies to escape attack by CD8+ CTLs. These include blocking processing and presentation of antigens by the class I MHC pathway and shutting down CD8+ T cell responses by inducing the phenomenon of exhaustion. These evasion mechanisms are discussed later in the chapter.

 

In latent infections, viral DNA persists in host cells, but the virus does not replicate or kill infected cells.

Latency is often a state of balance between infection and the immune response. CTLs generated in response to the virus can control the infection but are unable to eradicate it. As a result, the virus persists in infected cells, sometimes for the life of the individual. Such latent infections are common with Epstein-Barr virus and several other DNA viruses of the herpesvirus family. Reactivation of the infection is associated with expression of viral genes that are responsible for cytopathic effects and for spread of the virus. These cytopathic effects may include lysis of infected cells or uncontrolled proliferation of the cells. Any deficiency in the host immune response can result in failure to control reactivated latent infection.

 

 In some viral infections, tissue injury may be caused by CTLs.

Some degree of immunopathology accompanies host responses to many, perhaps most, virus infections. An experimental model of a disease in which the pathology is primarily due to the host immune response is lymphocytic choriomeningitis virus (LCMV) infection in mice, which induces inflammation of the spinal cord meninges. LCMV infects meningeal cells, but it is noncytopathic and does not injure the infected cells directly. The virus stimulates the development of virus-specific CTLs that kill infected meningeal cells during a physiologic attempt to eradicate the infection. Therefore, meningitis develops in normal mice with intact immune systems,

 

 

Immune Evasion by Viruses

Viruses can alter their antigens and are thus no longer targets of immune responses. The antigens affected are most commonly surface glycoproteins that are recognized by antibodies, but T cell epitopes may also undergo variation. The principal mechanisms of antigenic variation are point mutations and reassortment of RNA genomes (in RNA viruses), leading to antigenic drift and antigenic shift. These processes are of great importance in the spread of influenza virus. The two major antigens of the virus are the trimeric viral hemagglutinin (the viral spike protein) and neuraminidase. Viral genomes undergo mutations in the genes that encode these surface proteins, and the variation that occurs as a result is called antigenic drift. The segmented RNA genomes of various strains of influenza viruses that normally inhabit different host species can recombine in host cells, and these reassorted viruses can differ quite dramatically from prevalent strains (Fig. 16.9). Reassortment of viral genes results in major changes in antigenic structure called antigenic shift, which creates distinct viruses such as the avian flu or the swine flu viruses. Because of antigenic variation, a virus may become resistant to immunity generated in the population by previous infections. The influenza pandemics that occurred in 1918, 1957, and 1968 were due to different strains of the virus, and the H1N1 pandemic of 2009 was due to a strain in which the strands of the RNA genome were reassorted among strains endemic in

pigs, fowl, and humans. Subtler viral variants arise more frequently. There are so many serotypes of rhinovirus that vaccination against the common cold may not be a feasible preventive strategy. HIV-1, which causes AIDS, is also capable of tremendous antigenic variation due to a high error rate in reverse transcription of its RNA genome during viral reproduction (see Chapter 21). In these situations, prophylactic vaccination may have to be directed against invariant viral proteins.

 

Some viruses inhibit class I MHC–associated presentation of cytosolic protein antigens.

Some viruses produce molecules that inhibit the immune response.

 

Some chronic viral infections are associated with failure of CTL responses, called exhaustion, which allows viral persistence. Studies of a chronic infection with lymphocytic choriomeningitis in mice have shown that this type of immune deficit may result from persistent antigen stimulation leading to upregulation of T cell inhibitory receptors, such as PD-1 (programmed death 1, see Fig. 11.3). There is evidence for CD8+ T cell exhaustion in chronic human viral infections, including HIV and hepatitis virus infection

 

Viruses may infect and either kill or inactivate immunocompetent cells. The obvious example is HIV, which survives by infecting and eliminating CD4+ T cells, the key inducers of immune responses to protein antigens.

 

1.3.3. Vezano za Sars-CoV-2:

* T čelije:

Quote

• https://www.nature.com/articles/s41586-020-2550-z

• SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls

• Article
• Published: 15 July 2020

 

Memory T cells induced by previous pathogens can shape the susceptibility to, and clinical severity of, subsequent infections¹. Little is known about the presence of pre-existing memory T cells in humans with the potential to recognize SARS-CoV-2. Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in COVID-19 convalescents (n=36). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then showed that SARS-recovered patients (n=23) still possess long-lasting memory T cells reactive to SARS-NP 17 years after the 2003 outbreak, which displayed robust cross-reactivity to SARS-CoV-2 NP. Surprisingly, we also frequently detected SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients (n=37). SARS-CoV-2 T cells in uninfected donors exhibited a different pattern of immunodominance, frequently targeting the ORF-1-coded proteins NSP7 and 13 as well as the NP structural protein. Epitope characterization of NSP7-specific T cells showed recognition of protein fragments with low homology to “common cold” human coronaviruses but conserved amongst animal betacoranaviruses. Thus, infection with betacoronaviruses induces multispecific and long-lasting T cell immunity to the structural protein NP. Understanding how pre-existing NP- and ORF-1-specific T cells present in the general population impact susceptibility and pathogenesis of SARS-CoV-2 infection is of paramount importance for the management of the current COVID-19 pandemic.

 

** antitela:

https://twitter.com/GordanLauc/status/1282549222890405888

 

 

2. Ako koga interesuje... iz 2018:

Heterogeneity and longevity of antibody memory to viruses and vaccines

 

 

 

 

[Referent]

https://rs-lat.sputniknews.com/svet/202007171123029835-zasto-su-gojazni-posebno-rizicni-i-kako-lek-protiv-holesterola-pomaze-kovid-19-korona-pandemija-fenofibrat/

 

Šta kažu Njemci?

[wwww]

 

This new Harvard Uni study does not confirm previous widely published results from Europe that blood type affects serious Covid disease or even mortality. Only blood group 0 also has a reduced risk of infection in this study

The Harvard study is methodologically superior to previous studies because it summarizes well-documented cases from many clinics. Fits also the observation that many blacks have the supposedly protective blood group 0 but are known to often get very seriously ill

 

[Asterion]

Quote

 

 

više

 

 

 

 

 

Quote

više

 

Edited July 19, 2020 by Asterion

[Jataganac]

"S obzirom na to da je u toku ogromno kliničko ispitivanje, grupa u Oksfordu se nada, mada još nema nikakvih garancija, da prve vakcinacije počnu nešto pre Božića. Vakcina se već proizvodi na nekoliko lokacija u Evropi i Americi i, što je još važnije, u Serum institutu u Indiji. Dakle, već je u toku globalna proizvodnja vakcine, koja će biti upotrebljena ukoliko se klinička ispitivanja pokažu uspešnim", rekao je Vilijams za RTS.

[Sunshine State]

Jos jedna, potencijalno obecavajuca, terapija:

 

http://www.pharmatimes.com/news/synairgens_sng001_shows_strong_promise_in_covid-19_trial_1345119

 

An aerosol-based drug treatment could drastically reduce the number of new coronavirus patients dying from the disease or requiring intensive care, according to preliminary results released Monday by a British biotech firm.

In a randomised trial of 100 patients admitted to hospital with COVID-19, those who received an inhaled formula of the protein interferon beta were at 79 percent lower risk of developing severe disease compared to those who received a placebo.

They were also more than twice as likely to make a full recovery compared with the control group.

[Cyber]

7 hours ago, Ruby Rhod (koji lebdi) said:

"S obzirom na to da je u toku ogromno kliničko ispitivanje, grupa u Oksfordu se nada, mada još nema nikakvih garancija, da prve vakcinacije počnu nešto pre Božića. Vakcina se već proizvodi na nekoliko lokacija u Evropi i Americi i, što je još važnije, u Serum institutu u Indiji. Dakle, već je u toku globalna proizvodnja vakcine, koja će biti upotrebljena ukoliko se klinička ispitivanja pokažu uspešnim", rekao je Vilijams za RTS.

 

13. Jun 2020

AstraZeneca has reached an agreement with Europe’s Inclusive Vaccines Alliance (IVA), spearheaded by Germany, France, Italy and the Netherlands, to supply up to 400 million doses of the University of Oxford’s COVID-19 vaccine, with deliveries starting by the end of 2020. >>>

Edited July 20, 2020 by Cyber

[Vjekoslav]

On 7/15/2020 at 6:37 PM, Asterion said:

Ko napravi  efikasnu vakcinu/ lek protiv ovog virusa postaje besmrtan.

Znaš onu... Ko prvi devojci...

 

ako devojka u medjuvremenu ne nestane, sama od sebe. i to je moguce. 

[Div]

38 minutes ago, Vjekoslav said:

 

ako devojka u medjuvremenu ne nestane, sama od sebe. i to je moguce. 

 

Ma, samo neka pronađu vakcinu/lek, posle će lako pronaći odgovarajuću bolest.

 

[Asterion]

 

 

8 hours ago, Ruby Rhod (koji lebdi) said:

"S obzirom na to da je u toku ogromno kliničko ispitivanje, grupa u Oksfordu se nada, mada još nema nikakvih garancija, da prve vakcinacije počnu nešto pre Božića. Vakcina se već proizvodi na nekoliko lokacija u Evropi i Americi i, što je još važnije, u Serum institutu u Indiji. Dakle, već je u toku globalna proizvodnja vakcine, koja će biti upotrebljena ukoliko se klinička ispitivanja pokažu uspešnim", rekao je Vilijams za RTS.

 

Zamislite kolike su ovde pare u pitanju, kad  si mogu priuštiti ovakav raskoš.

[djura.net]

49 minutes ago, Asterion said:

 

 

 

Zamislite kolike su ovde pare u pitanju, kad  si mogu priuštiti ovakav raskoš.

I meni je to prvo palo na pamet, a onda razmisljam, zar ne bi trebalo da je zdravlje I ljudski zivot uvek na prvom mestu?

[Asterion]

57 minutes ago, djura.net said:

I meni je to prvo palo na pamet, a onda razmisljam, zar ne bi trebalo da je zdravlje I ljudski zivot uvek na prvom mestu?

 

To je svakakona prvom mestu. Previše je svega u igri, da bi se kockali sa ljudima.

 

Ja pričam o tome kako imaju ljude i opremu spremnu za zeleno svetlo iz (verovatno) Oksforda. Kad se završi ispitivanje. Samo ON.

 

Verovatno su sve tehničke probleme proizvodnje več sredili.

 

Ne znam tačno ni u čemu če se proizvoditi vakcina. Dio te platforme su u Oksfordu več imali, jer su se bavili sa nekim sličnim virusom od prije...

 

 

 

 

Virus je od majmuna. Pa je unutra stavljen jedan komadič genoma ovog 'našeg' virus. Kad se takav virus namnoži ima još jedan dio gor na sebi. To je taj dio od korone. 

 

Quote

 

The vaccine - called ChAdOx1 nCoV-19 - is being developed at unprecedented speed.

It is made from a genetically engineered virus that causes the common cold in chimpanzees.

bbc

 

 

Quote

The recombinant adenovirus for ChAdOx1 nCoV-19

Lancet

 

Zašto od šimpanza virus?

 

Quote

Non-human primate (NHP)-derived adenoviruses have formed a valuable alternative for the use of human adenoviruses in vaccine development and gene therapy strategies by virtue of the low seroprevalence of neutralizing immunity in the human population.

 

 

Quote

Chimpanzee adenoviral vectors are a very well-studied vaccine type, having been used safely in thousands of subjects, from 1 week to 90 years of age, in vaccines targeting over 10 different diseases.

Coronaviruses have club-shaped spikes on their outer coats. Immune responses from other coronavirus studies suggest that these are a good target for a vaccine. The Oxford vaccine contains the genetic sequence of this surface spike protein inside the ChAdOx1 construct. After vaccination, the surface spike protein of the coronavirus is produced, which primes the immune system to attack the coronavirus if it later infects the body. Prof. Gilbert and team have previously developed a vaccine for another human coronavirus disease, which is Middle East Respiratory Syndrome (MERS), and this has shown promise in early clinical trials.

 

 

 

 

Ti moraš te tako promenjene 'majmunske' viruse namnožiti u nekim čelijama. Te čelije moraš gojiti/čuvati da ne umru, da ne raste u tim biorekatorima još nešto drugo itd. Moraju rasti u pravim uslovima, da imaš dovoljno virusa. Morša non stop čekirati, da virus nije se promenijo, čelije nisu mutirale.

 

Posle kad imaš proizvod=modificirani majmunski virus=vakcina, ga moraš očistiti od tih čelija i ostalog u tim biorektorima.

 

Sve to mora biti sterilno (ne ono što Akira govori nego još puno puno više).

 

I posle se pune vijale, itd. 

 

 

 

 

 

Tu su u pitanju posle volumni...

 

Jedan od izazova je svakako kako napraviti, da iz te male T-flašice/biorekatora  dobivaš posle isto kvalitetan proizvod i željenoj količini/čistoči  i u velikm biorekatorima (uslovi rasta čelija,...).

 

Ovo je taj up-scalingo kojem pričam. Nisu uslovi za čelije isti kad raste u na levoj i desnoj strani.

 

Jedan od suradnika, Halix B.V....

 

Quote

Under the agreement, HALIX B.V. will utilise its 1,000 L single use bioreactor suite within its 6,700 m² BSL2 GMP facility, located in Leiden, to transfer an industrial scale drug substance process from Pall in the UK, supporting the manufacture of ChAdOx1 nCoV-19 clinical trial material. Based on this transfer, HALIX B.V. and the consortium will be in a position to manufacture at a larger scale.

 

 

Primer (nije vezano na gornji quote) kako izgledaju ti posebni prostori:

 

 

 

Edited July 20, 2020 by Asterion

[Asterion]

Performing Arts Aerosol Study Round one preliminary results Clarinet, Flute, Horn, Soprano Singer, Trumpet

[Asterion]

July 17, 2020

 

 

 

Ima i u obliki podcast-a: KLIK

[CheshireCat]

Quote

Vakcina se već proizvodi na nekoliko lokacija u Evropi i Americi i, što je još važnije, u Serum institutu u Indiji. Dakle, već je u toku globalna proizvodnja vakcine, koja će biti upotrebljena ukoliko se klinička ispitivanja pokažu uspešnim", rekao je Vilijams za RTS.

 

 

Koja je šansa da se ovakva investicija propadne. Koja je šansa da se vakcina pokaže kao nedelotvorna?

[Kronostime]

52 minutes ago, CheshireCat said:

 

 

Koja je šansa da se ovakva investicija propadne. Koja je šansa da se vakcina pokaže kao nedelotvorna?

Velika, pogotovo zato sto je virus u medjuvremenu mutirao.

[ZiS]

Potpuni sam laik ali kapiram da oni prate i te mutacije i da one nisu toliko drasticne da bi vakcinu ucinile beskorisnom...

[Jataganac]

Ne bi se neko za*ebavao da vec krece sa stancanjem tolikih doza da nije siguran da ce to biti ok. Jasno je njima da ona radi pos'o, samo mora da prodje testiranja i minimum procedure.

[Laki21]

https://www.b92.net/zdravlje/vesti.php?yyyy=2020&mm=07&dd=21&nav_id=1709263

[Jataganac]

https://www.fiercepharma.com/pharma/astrazeneca-signs-covid-19-shot-deal-russia-days-after-hacking-accusations-surface

 

I u Rusiji ce se stancati Oxford/AstraZeneca vakcina.