There was a simultaneous outbreak of the zoonotic Nipah henipavirus in Wuhan - 4 out of 5 patients have the virus in Jinyintan Hospital , along with SARS-Cov2, in their metagenome - which seems to have resolved by itself

2020 ◽  
Author(s):  
Sandeep Chakraborty

‘Nipah virus is a biosafety level 4 (BSL-4) pathogen that causes severe respiratory illness and encephalitis in humans’ [1] that orginates in bats [2]. It was first isolated in Malaysia and Singapore in 1999 - ‘late September 1998 and by mid-June 1999, more than 265 encephalitis cases, including 105 deaths, had been reported in Malaysia, and 11 cases of encephalitis or respiratory illness with one death had been reported in Singapore’ [3]. It keeps recurring in Bangladesh [4]. There was a 2018 outbreak in Kerala, India [5]. There seems to have been a simultaneous outbreak in Wuhan during Covid19 - which never got reported, and apparently resolved by itself.Metagenome from the bronchoalveolar lavage fluid of 5 Covid19 [6–8] patients from Wuhan (Accid:PRJNA605983) which showed very little SAR-Cov2 viral load (in the tens per million reads) in my analysis earlier [9].The metagenome also shows the co-infection with Nipah henipavirus virus in 4 out of 5 patients. The sequences are in SI:Nipah.fa - 167 reads in all.One can almost assemble the full genome (about 18kbps) from it. It seems to have originated from Bangladesh, though I have not done the phylogeny. Most reads are 100% identical, but some are (97% - 145/150).Maybe, we have looking for the wrong virus in the rest of the world - since Nipah is endemic to Southeast Asia, which seems to have been the least affected in Covid19.

2015 ◽  
Vol 2 (suppl_1) ◽  
Author(s):  
Isabelle Paula Lodding ◽  
Hans Henrik Schultz ◽  
Jens Ulrik Jensen ◽  
Claus Andersen ◽  
Michael Perch ◽  
...  

1997 ◽  
Vol 27 (4) ◽  
pp. 396-405 ◽  
Author(s):  
L. M. TERAN ◽  
M. G. CAMPOS ◽  
B. T. BEGISHVILLI ◽  
J.-M. SCHRODER ◽  
R. DJUKANOVIC ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  

Abstract Background Senicapoc is a potent and selective blocker of KCa3.1, a calcium-activated potassium channel of intermediate conductance. In the present study, we investigated whether there is a beneficial effect of senicapoc in a large animal model of acute respiratory distress syndrome (ARDS). The primary end point was the PaO2/FiO2 ratio. Methods ARDS was induced in female pigs (42–49 kg) by repeated lung lavages followed by injurious mechanical ventilation. Animals were then randomly assigned to vehicle (n = 9) or intravenous senicapoc (10 mg, n = 9) and received lung-protective ventilation for 6 h. Results Final senicapoc plasma concentrations were 67 ± 18 nM (n = 9). Senicapoc failed to change the primary endpoint PaO2/FiO2 ratio (senicapoc, 133 ± 23 mmHg; vehicle, 149 ± 68 mmHg). Lung compliance remained similar in the two groups. Senicapoc reduced the level of white blood cells and neutrophils, while the proinflammatory cytokines TNFα, IL-1β, and IL-6 in the bronchoalveolar lavage fluid were unaltered 6 h after induction of the lung injury. Senicapoc-treatment reduced the level of neutrophils in the alveolar space but with no difference between groups in the cumulative lung injury score. Histological analysis of pulmonary hemorrhage indicated a positive effect of senicapoc on alveolar–capillary barrier function, but this was not supported by measurements of albumin content and total protein in the bronchoalveolar lavage fluid. Conclusions In summary, senicapoc failed to improve the primary endpoint PaO2/FiO2 ratio, but reduced pulmonary hemorrhage and the influx of neutrophils into the lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment to reduce alveolar neutrophil accumulation and improve long-term outcome in ARDS.


Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S286
Author(s):  
Guzin Gursoy ◽  
Sibel Alpar ◽  
Nazire Ucar ◽  
Tulay Bakirci ◽  
Ahmet Aydin ◽  
...  

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