Kinų mokslininkai patvirtino, kad COVID-19 turi ŽIV viruso intarpus

Prancūzų virusologas, Nobelio premijos laureatas Luc Antoine Montagnier, kuriam ši premija suteikta 2008 metais už jo 1983 metais atrastą ŽIV virusą, balandžio vidury pareiškė, kad SARS-CoV-2 sukurtas laboratorijoje.

„Jis ne natūralios kilmės, tai molekulinių biologų darbas“, – mano mokslininkas. Montagnier nieko nekaltino ir nežino, kas galėjo „surinkti“ naują virusą. „Gali būti, jie norėjo sukurti vakciną prieš AIDS“, – pasakė jis.

https://www.zerohedge.com/health/coronavirus-uses-same-strategy-hiv-evade-immune-response-chinese-study-finds

Mainstriminė MIP ėmė šaipytis iš mokslininko, įžeidinėti, o kai kurie kolegos jo nuomone neigti.

Gegužės 24 dieną Cold Springs Harbos laboratorijos preprintų serveryje Biorxiv kinų mokslininkų kolektyvas paskelbė straipsnį, patvirtinantį, kad Sars-CoV-2 genome yra „ŽIV insercijos“. Būtent tai, ką anksčiau tvirtino ŽIV viruso atradėjas Luc Antoine Montagnier. Šis tyrimas patvirtina, kad COVID-19 yra dirbtinai sukurtas virusas! Jis naudoja tą pačią strategiją, kaip ir ŽIV, kad įveikti žmogaus imuninę sistemą.

Šis darbas – paskutinė vinis į „konspirologinių teorijų“ cenzorių karstą, kuriems aš jau esu pasiūlęs, pasiremdamas daugybe anksčiau skelbtų mokslinių faktų, „susikišti savo liežuvius į užpakalius“. Gal reikėtų tai padaryti ir ponui Cukerbergui, ponui Geitsui ir jų sėbrams, juk jie yra šios beprotiškos cenzūros organizatoriai.

Serveryje pateikiamas visas straipsnis. Aš, dėl viso pikto, pateikiu jo reziumė:

https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1

The ORF8 Protein of SARS-CoV-2 Mediates Immune Evasion through Potently Downregulating MHC-I

ProfileYiwen Zhang, Junsong Zhang, Yingshi Chen, Baohong Luo, Yaochang Yuan, Feng Huang, Tao Yang, Fei Yu, Jun Liu, Bingfen Liu, Zheng Song, Jingliang Chen, Ting Pan, Xu Zhang, Yuzhuang Li, Rong Li, Wenjing Huang, Fei Xiao, Hui Zhang

Summary

SARS-CoV-2 infection have caused global pandemic and claimed over 5,000,000 tolls1–4. Although the genetic sequences of their etiologic viruses are of high homology, the clinical and pathological characteristics of COVID-19 significantly differ from SARS5,6. Especially, it seems that SARS-CoV-2 undergoes vast replication in vivo without being effectively monitored by anti-viral immunity7. Here, we show that the viral protein encoded from open reading frame 8 (ORF8) of SARS-CoV-2, which shares the least homology with SARS-CoV among all the viral proteins, can directly interact with MHC-I molecules and significantly down-regulates their surface expression on various cell types. In contrast, ORF8a and ORF8b of SARS-CoV do not exert this function. In the ORF8-expressing cells, MHC-I molecules are selectively target for lysosomal degradation by an autophagy-dependent mechanism. As a result, CTLs inefficiently eliminate the ORF8-expressing cells. Our results demonstrate that ORF8 protein disrupts antigen presentation and reduces the recognition and the elimination of virus-infected cells by CTLs8. Therefore, we suggest that the inhibition of ORF8 function could be a strategy to improve the special immune surveillance and accelerate the eradication of SARS-CoV-2 in vivo.

Since the outbreak of COVID-19, the disease has been spreading around the world rapidly1–4. Although both COVID-19 and SARS cause severe respiratory illness, the epidemiological and clinical data suggest that the disease spectrum of COVID-19 significantly differ from that of SARS: COVID-19 shows longer incubation period, which is around 6.4 days, ranged from 0 to 24 days; the interpersonal transmissions could occur from pre-symptomatic individuals5,6; asymptomatic infection has been widely reported for COVID-19 and severely jeopardize the prevention system in a community5; a significant portion of recovered patients still keep shedding viral genetic substances in upper respiratory tract and digestive tract, leading to their stay in the hospital for a significant long time9–11; a certain amount of recovered patients turn to re-detectable viral RNA positive after discharge from the hospital12. The desynchronization of viral titer and clinical symptom development suggest that the etiologic agent SARS-CoV-2 could have undergone extensive replication in infected host cells without being effectively monitored by host anti-viral immunity.

Cytotoxic T lymphocytes (CTLs) are important for the control of viral infections by directly eradicating the virus-infected cells. In a virus-infected cell, MHC-I molecules present peptides derived from a variety of viral proteins. Once the T cell receptor on CD8+ T cells recognizes the special signal presented by MHC-I-peptide complex, the CTL releases various toxic substances including perforins, granzyme, and FasL which directly induce the death of viral-infected cells, as well as many other cytokines such as interferon-γ, TNF-α, and IL-2, etc8. As a result, the cells supporting the viral replication will be eradicated and the spread of viruses will be effectively prevented13. Some viruses leading to chronic infection, such as human immunodeficiency virus type 1 (HIV-1) and Kaposi’s sarcoma-associated herpesvirus (KSHV), can disrupt antigen presentation for immune envision by down-regulating MHC-I on the surface of cells and evading the immune surveillance14–16. Given that SARS-CoV-2 exerts some characteristics of viruses causing chronic infection, we hypothesize that the viral protein(s) of SARS-CoV-2 may affect the antigen presentation system and assist the viruses to escape from immune surveillance.