Maria be careful about interruption or you become Hannity
She is host she controls.
most hosts give time limit when the guest is abusing time.
not likely enterovirus is very different.
Red dawn Maria
No intestinal and very mild usually
and not much genome cross over.
https://en.wikipedia.org/wiki/Enterovirus
no entero viruses are primarily fecal oral.
Maria is pissed at China
Medical Anon here:
retrovirus is basically foot and mouth. On rare occasion it may cause respiratory signs but those are usually secondary to intestinal signs and pico corona is just the same thing as corona virus.
opps auto correct enterovirus
enterovirus is totally not even close to corona virus
not even close.
Nunes will be the next american president if he can convince Pompeo to be BP
Nunes/Pompeo ticket 2024
Maria Tracker I noted it
Maria touched on COVID tracker on your phones.
Maria this moronic talk of vaccine for COVID19 is just distraction
A vaccine will never work on this virus.
COVID 19 virus is not a vaccine candidate it is primarily an immune modulating virus and those vaccines make worse =
no go.
COVID 19 is a bio weapon that got out of China.
that is solid now.
What is up in the air is if it is chronic or just a Spanish flu thing.
Evidence shows "re-infection" etc and measles like R0 level.
But no great fix actually if that is true.
I feel sorry for all those young that allow themselves to get infected believing the MSM. Because this is herpes flu,.
Medical evidence shows that that COVID-19 invades and infects T cells killing some and lying in wait in those that not killed - it also causes changes in antibody production of B lymphocytes. This is a very well designed virus.
and we will not get the true illness for 2-3 years.
do I really have to dig it up again over and over?
2007 Paper by Chi Scientists on how they would make the bioweapon corona mixed with HIV – COVID
https://jvi.asm.org/content/jvi/early/2007/12/12/JVI.01085-07.full.pdf
COVID19 in Spleen and Lymph nodes and the 169+ Macrophage and Lymphocyte damage:
https://www.medrxiv.org/content/10.1101/2020.03.27.20045427v1
More on CD169+ Macrophage and how it works:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6212557/
Cats and Ferrets highly susceptible to COVID19, shows infection spread between them:
https://science.sciencemag.org/content/early/2020/04/07/science.abb7015
OFR8 the part (nonfunctional0 area of SARS investigations to change to make SARS more infectious:
https://academic.oup.com/jid/article/213/4/579/2459467
https://www.ncbi.nlm.nih.gov/pubmed/26269185
2015 Paper on Corona Viruses and how to make them a Pandemic:
https://www.nature.com/articles/nm.3985
TMPRSS2 Mechanism part of pathogenesis for COVID19:
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/tmprss2
More on Pseudo HIV
https://www.sciencedirect.com/science/article/abs/pii/S0166093407003254
Lymphocyte and Cytokine response to COVID
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7165294/
Immune changes in COVID19
https://www.tandfonline.com/doi/full/10.1080/22221751.2020.1746199
Lymphocyte death in COVID19 and sepsis
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30920-X/fulltext
COVID19 infect T Lymphocytes:
https://www.nature.com/articles/s41423-020-0424-9
Pathogenic T cells and inflammatory monocytes incite inflammatory storm in severe COVID-19 patients
https://watermark.silverchair.com/nwaa041.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAmswggJnBgkqhkiG9w0BBwagggJYMIICVAIBADCCAk0GCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMF6W8b0w-b2YKqSzDAgEQgIICHntq0ZkXz9tobPCeMJapgsAuPYBKl7SVX8iWVVBp1j66S-FMLJvZ3UCBq6D9ORdw1STi-GYaFpMqEIJaMoINFzAdLbLf6bAUmWgXppOYawPzDDO2gbqIW5CtSAoHC_cwD3LMeXw7rVotZx4ZWjXdNlqvLDJWaw6PVjFm3p_uaKkpA6tHCstd3-xSXud9ZFYB-caizZIqfaRy_Yv5dmQQYxWXjFDxcNZxjyQ2tE-Q2k83yB4Bca6BgFxl4rpcp0DTgZE5IrJrxiGCLh-QMnLQXHGsJNuJhB7l66_UgBOC0GRS6dW0vlCKbUjmDrk-D7QReYEsGoolB4w_Vb2l81SS3hfkccuSKajZLa-92c0F9f6Q2sECOXLUa0Juy8LR4ORJSkh4o5va_DLMtWxoIlIjKe6Vicea1fnUdbgZbEsBQGhBbJSMIKQirt5cj7O3cb9bUvI2Pc6gLMytu69jj-8VNtluc0jHHY1Pk4mnUlXFRkM9FdF6Ye-v2BEQLap1v_KUWJRk4vT2_2daHOxEMINaOpzr67APkld1sjyfhqCF70yhNb2hZE8HGF4G2amH1nrQZo1Mf4ioYc3N23JSLC-V9E_NHGQ7eFKWvqoFUjFVVXsNPfvmg6PgUvY6QbD6MvScC_Va5kYyWOv6PEL7QuT_lKR9uKxdvOzZYXigXFJ6VScZGD8INjz6NXBPw_1YXl37WlceCGvDMMDUK3wHveW_
Coronavirus could attack immune system like HIV by targeting protective cells
https://www.scmp.com/news/china/society/article/3079443/coronavirus-could-target-immune-system-targeting-protective
Please note 2 of these scholarly articles say bad antibody response and one says good.
No evidence antibodies protect against COVID19.
https://time.com/5827450/who-coronavirus-antibodies-reinfection/
science studies:
https://www.ncbi.nlm.nih.gov/pubmed/32221519
The potential danger of suboptimal antibody responses in COVID-19
https://www.nature.com/articles/s41577-020-0321-6
Temporal profiles of viral load in posterior oropharyngeal saliva samples and serum antibody responses during infection by SARS-CoV-2
https://www.sciencedirect.com/science/article/pii/S1473309920301961
Conclusion no neutralizing antibodies in natural infection
Neutralizing Antibodies against SARS-CoV-2 and Other Human Coronaviruses
https://www.sciencedirect.com/science/article/pii/S1471490620300570
Human monoclonal antibody to COVID19
https://www.nature.com/articles/s41423-020-0426-7
no no lots of evidence.
lots of evidence out there - just another:
nature.com/articles/s41423-020-0483-y
Systemically comparing host immunity between survived and deceased COVID-19 patients
basically T lymphocytes are targeted by COVID 19 and:
copy paste:
nature.com/articles/s41423-020-0483-y
Systemically comparing host immunity between survived and deceased COVID-19 patients
Since dysregulation of immune responses and temporal dynamics in T-cell activation have been noted in patients with COVID-19,4,7,8 we thus classified the patients into early (≤10 days), middle (11–20 days), late (21–30 days), and end (>30 days) stages of disease based on the time from symptom onset. The numbers of cases in the early, middle, late, and end stages were 5, 23, 33, and 34 in survived patients, and were 5, 12, 32, and 13 in deceased patients, respectively. Generally, deceased patients demonstrated higher number of neutrophils and lower number of lymphocytes compared to survived patients (Supplementary Table 2).
To gain greater insight into the kinetics of immune cells, flow cytometry was performed to explore the number, phenotype, and function of T, B, and dendritic cells (DC) as well as monocytes in survived and deceased patients (Supplementary Fig. 1). Although a comparable CD4+ T-cell count was noted between survived and deceased patients in the early stage, deceased patients displayed dramatically lower CD4+ T-cell count than survived patients in the middle and late stages, indicating the distinct immune response kinetics between two groups (Fig. 1a). We next examined the activation and effector function of CD4+ T cells by analyzing HLA-DR expression and IFN-γ producing ability. We found that the frequencies of HLA-DR+ and IFN-γ+ cells within CD4+ T cells were markedly increased in the middle stage compared to those in the early stage, which then rapidly declined in the late stage and kept a low level in the end stage in decreased patients (Fig. 1a). However, the frequencies of HLA-DR+ and IFN-γ+ cells within CD4+ T cells in survived patients continuously increased after symptom onset, and maintained at a certain level in the late and end stages (Fig. 1a). Thus, decreased patients demonstrated much higher frequency of HLA-DR+ cells within CD4+ T cells than survived patients in the middle stage, whereas both HLA-DR expression and IFN-γ producing ability of CD4+ T cells in the late stage in deceased patients were significantly lower than those in survived patients (Fig. 1a). Moreover, lower CD45RO expression on CD4+ T cells was noted, again, in deceased patients in comparison with that in survived patients in all stages (Fig. 1a). However, the expressions of CD45RA and CD28 on CD4+ T cells in the late and end stages were significantly higher in deceased patients than those in survived patients (Fig. 1a).