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16th May 2020, 16:54 |
#1
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Mania Member
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Studi: Ada Yang Sudah Duluan Punya Kekebalan Terhadap Virus COVID-19...
Sebagian dari sampel-sampel yang di dapat dan di-studi oleh para peneliti ini ternyata menunjukkan telah adanya "pre-existing immunity" terhadap virus COVID-19.
Abstract Several related human coronaviruses (HCoVs) are endemic in the human population, causing mild respiratory infections. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiologic agent of Coronavirus disease 2019 (COVID-19), is a recent zoonotic infection that has quickly reached pandemic spread. Zoonotic introduction of novel coronaviruses is thought to occur in the absence of pre-existing immunity in the target human population. Using diverse assays for detection of antibodies reactive with the SARS-CoV-2 Spike (S) glycoprotein, we demonstrate the presence of pre-existing immunity in uninfected and unexposed humans to the new coronavirus. SARS-CoV-2 S-reactive antibodies, exclusively of the IgG class, were readily detectable by a sensitive flow cytometry-based method in SARS-CoV-2-uninfected individuals with recent HCoV infection and targeted the S2 subunit. In contrast, SARS-CoV-2 infection induced higher titres of SARS-CoV-2 Sreactive IgG antibodies, as well as concomitant IgM and IgA antibodies throughout the observation period of 6 weeks since symptoms onset. HCoV patient sera also variably reacted with SARS-CoV-2 S and nucleocapsid (N), but not with the S1 subunit or the receptor binding domain (RBD) of S on standard enzyme immunoassays. Notably, HCoV patient sera exhibited specific neutralising activity against SARS-CoV-2 S pseudotypes, according to levels of SARS-CoV-2 S-binding IgG and with efficiencies comparable to those of COVID-19 patient sera. Distinguishing pre-existing and de novo antibody responses to SARS-CoV-2 will be critical for serology, seroprevalence and vaccine studies, as well as for our understanding of susceptibility to and natural course of SARS-CoV-2 infection. ... Conclusions Cross-reactivity between seasonal HCoVs and the pandemic SARS-CoV-2 needs to be carefully considered in the development and interpretation of assays for precise detection of SARS-CoV-2-specific antibodies. The flow cytometry-based method we employed demonstrated the highest degree of specificity and sensitivity. A similar method was also recently used in an independent study, reaching comparable results, except no cross-reactivity with HCoV was suggested. Although not specifically investigated in the latter study, detection of cross-reactivity with HCoV was deliberately avoided by higher dilution of serum samples. Whilst clearly detectable, titres of SARSCoV-2 S-reactive antibodies are one order of magnitude lower in HCoV patient sera than in COVID-19 patient sera and drop below detection limits upon further serum dilution also in our assay. Running the assay in sensitive mode still allows the distinction between pre-existing and de novo antibody responses to SARS-CoV-2, based on the levels of SARS-CoV-2 S-reactive IgG and parallel detection of IgM and IgA. These distinguishing features were maintained and, indeed, appear to increase during the first 43 days post onset of COVID-19 symptoms (the latest time-point we have examined). It is possible that these features are maintained for longer periods post SARS-CoV-2 infection, but it is also expected that the discriminating ability will be lost over time. Increasing specificity of the assays will be at expense of sensitivity. This is evident in the use of more variable SARS-CoV-2 protein domains such as S1 and RBD, which exhibited approximately 85% sensitivity during the first 43 days post onset of COVID-19 symptoms in our study, and which is likely to drop further with waning antibody titres over longer periods. The apparent ability of HCoV patient sera to neutralise SARS-CoV-2 S pseudotypes raise similar concerns regarding the specificity of neutralisation assays. For example, 5 of 1,000 samples from healthy Scottish blood donors collected in March 2020 neutralised SARS-CoV-2 S pseudotypes and 1 or 100 of samples collected in 2019 also had neutralising activity in the absence of a strong ELISA signal. Notably, these samples were described to have low or no SARS-CoV-2 S-reactive IgM antibodies, a feature we would associate with immune memory of HCoVs. In addition to its implications for serology assay development and interpretation or for the design of vaccination studies, potential cross-reactivity between seasonal HCoVs and the pandemic SARS-CoV2 has important ramifications for natural infection. Thorough epidemiological studies of HCoV transmission suggest that cross-protective immunity is unlikely to be sterilising or long-lasting, which is also supported by repeated reinfection of all age groups, sometimes even with homologous HCoVs33. Nevertheless, prior immunity induced by one HCoV has also been reported to reduce the transmission of homologous and, importantly, heterologous HCoVs, and to ameliorate the symptoms where transmission is not prevented. A possible modification of COVID-19 severity by prior HCoV infection might account for the age distribution of COVID-19 susceptibility, where higher HCoV infection rates in children than in adults correlates with relative protection from COVID-19. Public health measures intended to prevent the spread of SARS-CoV-2 will also prevent the spread of and, consequently, maintenance of herd immunity to HCoVs, particularly in children. It is, therefore, imperative that any effect, positive or negative, of pre-existing HCoV-elicited immunity on the natural course of SARS-CoV-2 infection is fully delineated. ======= Yang belum diketahui adalah sejauh mana "pre-existing immunity" ini memberikan perlindungan terhadap serangan dari strain-strain COVID-19. Tetapi ini ikut menjelaskan tentang daerah-daerah tertentu yang kelihatannya tidak mengalami serangan hebat dari COVID-19 padahal secara kontinyu terus berbaur dengan populasi-populasi tertentu yang dianggap merupakan carrier dari virus COVID-19. Bali kemungkinan salah satu wilayah yang populasinya mempunyai "pre-existing immunity" ini, yang memberikan mereka imunitas parsial terhadap COVID-19. - https://www.biorxiv.org/content/10.1...414v1.full.pdf |
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16th May 2020, 18:48 |
#2
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Mania Member
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berati benar donk kebijaksanaan wiwi yang membuka pariwisata seluas luasnya pada saat covid mulai di china. sehingga yg datang adalah yg membawa virus awal yg jinak dan membuat herd imunity di bali dan beberapa daerah lain di indonesia...
padahal para kadrun nyinyir berat di forum ini, tenyata maksud baik orang lebih diberkati Tuhan daripada iblis yg berlindung dibalik kedok agama. karena Tuhan punya rencana sendiri yg menyebabkan iblis dipermalukan pada ahirnya... |
16th May 2020, 18:52 |
#3
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Groupie Member
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Quote:
Harusnya bila tidak ada kekebalan yg terbentuk di masyarakat atau individu maka sudah puluhan ribu orang meninggal krn covid ini. Contoh konkritnya ada di member forpol yg ngakunya sudah menjadi ODP berbulan2 dan tinggal dwngan pasien positif ternyata sampe hari ini statusnya masih ODP negatif..hanya sayang secara mental agak terganggu karena mungkin faktor stress atau depresi. |
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16th May 2020, 20:57 |
#4
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Mania Member
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Masalahnya sebagian org yg kena covid bisa mati dlm waktu singkat. Termasuk usia muda. Contoh siapa tuh penyanyi tdk terkenal yg barusan meninggal mggu lalu. Usia masih di 30 apa kurang.
Org kena hiv aja masih positif berpuluh tahun sampe tiba2 aids. Jd covid mmg lbh ganas tapi anehnya ada yg kebal, |
16th May 2020, 21:51 |
#5
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Groupie Member
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Quote:
Coronavirus manusia itu penyebab penyakit pilek biasa/ringan. Jadi bukan pernah terkena COVID-19 ringan yang memberikan kekebalan tapi pernah kena pilek biasa/ringan yang mungkin membuat ada kekebalan sebelum masuknya COVID-19. Yang jadi pertanyaan saya adalah yang kebal itu yang sering pilek atau yang tidak pernah pilek? Kalau yang sering pilek, saya mungkin beruntung. Kalau yang tidak pernah pilek, saya ini sangat tidak beruntung karena sering pilek dan batuk. Mungkin sering pilek dan batuk tanda saya ini sangat lemah terhadap coronavirus jadi lebih besar resiko kena virus coronavirus yang penyebab COVID-19. |
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King of Losers Last edited by kumalraj; 16th May 2020 at 21:54.. |
16th May 2020, 22:25 |
#6
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Mania Member
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Quote:
Lagi-lagi pernyataan menyepelekan nyawa: "belum ada kematian massal", tapi di negara ini dari yang positif saja sudah ada 1.000an, yang ODP 3.000an yang meninggal. Ini bukan data dari Anies ya, ini data dari KawalCovid19. Kok nyepelein banget gitu, 4.000an nyawa terbuang kau anggap biasa. Okelah kalau penyebabnya natural, lah ini karena sejak awal pemerintah juga nyepelein dengan statement blunder: kita sudah kebal karena makan nasi kucing dan minum jamu. Dan bukti nyata, hingga saat ini rate test kita setara negara-negara miskin di Afrika. Padahal sudah 2 bulan sejak kasus positif pertama di awal Maret tapi kok masih segini aja. Covid-19 membuka semua kebobrokan negara kita, terutama mutu kesehatan yang sangat buruk dan masyarakat yang susah diatur. |
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16th May 2020, 23:32 |
#7
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Mania Member
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Quote:
Tiap kali Dikeroyok buzzer amatir |
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17th May 2020, 00:00 |
#8
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Mania Member
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Sebenarnya studi yang ini ikut menguatkan hasil studi yang sebelumnya dari sekelompok peneliti yang dipimpin oleh sekelompok ahli epidemiologi dari "Charite - Universitatsmedizin Berlin".
Studi yang disebarkan sekitar sebulan yang lalu tersebut juga menyatakan adanya "pre existing immunity" terhadap virus Covid-19. Riset mereka menitik-beratkan kepada terdapatnya "S-reactive CD4+ T-Cell" pada 83% penderita COVID-19, tetapi ternyata ini terdapat juga pada 34% sampel dari orang-orang yang sehat padahal mereka belum pernah terkena COVID-19. Ini menunjukkan ada sebagian populasi yang memang sudah "mengenal", atau terbangun imunitas nya, walaupun belum sempat terjangkit COVID-19. ... Discussion Our study demonstrates the presence of S-reactive CD4+ T cells in COVID-19 patients, and in a subset of SARS-CoV-2 seronegative HD. In light of the very recent emergence of SARS CoV-2, our data raise the intriguing possibility that pre-existing S-reactive T cells in a subset of SARS-CoV-2 seronegative HD represent cross-reactive clones raised against S-proteins, probably acquired as a result of previous exposure to HCoV. Endemic HCoV account for about 20% of "common cold" upper respiratory tract infections in humans. HCoV infections are ubiquitous, but they display a winter seasonality in temperate regions. Based on epidemiological data indicating an average of two episodes of "common cold" per year in the adult population, it may be extrapolated that the average adult contracts a HCoV infection on average every two to three years. Protective antibodies may wane in the interim but cellular immunity could remain . Although the overall amino acid sequence homology of spike glycoproteins is relatively low among HCoV, there is an overlap of MHC-II epitopes located especially in the C-terminal domain of the here used peptide pools (Figure 1a, Supplementary Figure 1). This may explain the preferential reactivity of CD4+ T cells to the C-terminal domain in one third of SARS-CoV-2 seronegative HD. The biological role of pre-existing SARS-CoV-2 S-cross-reactive CD4+ T cells in 34% of HD remains unclear for now. However, these cells may represent the key to understanding the vastly divergent manifestations of SARS-CoV-2 disease courses, and particularly the suspected high rate of asymptomatic infections in children and young adults assuming that these S-crossreactive CD4+ T cells have a protective role in SARS-CoV-2 infection. Since children and young adults have on average more frequent social contacts than the elderly, one might expect a higher transmission rate and HCoV prevalence in the former. This assumption would need to be investigated in future longitudinal studies assessing the presence of pre-existing SARS-CoV2-cross-reactive CD4+ T cells and their impact on the susceptibility to SARS-CoV-2 infection and age-realted clinical outcomes of COVID-19. SARS-CoV neutralizing antibodies are associated with convalescence, and they have been detected 12 months after disease. However, the durability of neutralizing antibody responses against SARS-CoV-2 currently remains unknown. Antibodies against HCoV can wane within months after infection, although HCoV re-infection is accompanied by low-level and shortlived virus shedding with only mild symptoms of short duration pointing towards residual immunity. Cellular immunity has not yet been studied in this context. The extent to which and how SARS-CoV-2 specific humoral or cellular immunity mediates durable protection against reinfection is unknown but will be one of the critically important fields of research in the coming months. It has been demonstrated in mouse models that CD4+ as well as CD8+ T cell responses directed against structural proteins such as spike or nucleocapsid protein of SARS-CoV critically contribute to viral clearance. To our knowledge, this study represents the first report of cellular SARS-CoV-2-cross reactivity in human T cells. Our results provide a decisive rationale to initiate worldwide prospective studies to assess the contribution of pre-existing SARS-CoV-2-cross-reactive immunity (potential regional differences) to clinical outcomes of SARS-CoV-2-infections. Together with currently introduced, novel serology tests, the data generated by such studies may critically inform evidence-based risk evaluation, patient monitoring, adaptation of containment methods, and last but not least, vaccine development. ======= - https://www.medrxiv.org/content/10.1...440v1.full.pdf |
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17th May 2020, 00:31 |
#9
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Mania Member
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Quote:
Jadi kuncinya bukan wajib melakukan berjuta-juta tes, karena bisa saja test yang sebanyak itupun ternyata masih belum memenuhi standar WHO yang diatas. Coba lihat tabel sederhana dari data-data COVID-19 sore tadi... Ternyata ada negara-negara yang telah melakukan berjuta-juta test belum memenuhi standar kecukupan test WHO. USA [11 juta test], Spanyol [2.5 juta test] dan Perancis [1.4 juta test] belum memenuhi kriteria kecukupan tes WHO. Demikian juga Singapura, Brazil dan Swedia belum memenuhi kriteria tersebut. Didalam tabel sederhana diatas, hanya Indonesia dan Turki yang memenuhi kriteria dari WHO tersebut, karena masing-masing negara tersebut hasil test positif nya kurang dari 10% dari jumlah tes yang dilakukan. |
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17th May 2020, 08:33 |
#10
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Groupie Member
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Kalau lihat tabel diatas, saya lebih milih seperti Singapura. Biarpun kasus positif yang terdeteksi jauh lebih banyak dari Indonesia, tapi kematian jauh lebih kecil.
Jadi terlihat testing benchmark WHO itu mungkin patokan yang tidak cocok. Ada kemungkinan Indonesia memenuhi benchmark justu karena testingnya terlalu sedikit. Bisa saja sebelum orangnya dapat giliran ditest sudah sembuh. Jadi yang negatif itu mungkin sebagian besar adalah yang sudah sembuh. Masuk akal karena kalau lihat angka kesembuhan Indonesia itu kecil kalau dibanding negara lain. Mungkin banyak yang tidak terhitung karena dianggap negatif atau tidak pernah tertular. |
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