scholarly journals Hyperenzymemia after vaccination against COVID-19: complex equation with simple variables

Author(s):  
L. Yu. Ilchenko ◽  
I. G. Fedorov ◽  
G. G. Totolyan ◽  
A. M. Karelina ◽  
G. A. Sedova ◽  
...  

The article presents clinical case of the jaundice development and severe hyperenzymemia in GAM-Covid-VAK (Sputnik V) vaccination against COVID-19 in a 69-year-old patient. History — systematic use of non-steroidal anti-inflammatory drugs due to persisting pain after knee arthroplasty in 2018; frequent trips for several years to another region for sanatorium treatment, the use of mineral water. The diseases caused by hepatitis viruses, drug damage and post-vaccination reaction were included in diagnostic search. The markers of hepatitis B and C infection viruses were not detected during the enzyme immunoassay and polymerase chain reaction. The indicator for determining the relationship of a drug with the liver damage development was 6 points (borderline value) and only indicated the likelihood of drug hepatotoxicity. At the same time, it is known from history that repeated administration of the drug did not cause liver dysfunctions. The diagnosis of coronavirus infection was established based on the identification of SARS-CoV-2 in the hospital with repeated laboratory testing and competing diagnosis of hepatitis A has been confirmed on the basis of hepatocellular damage and the presence of serological marker of hepatitis A virus (immunoglobulin M antibodies). The treatment was continued in the infectious hospital, where the diagnosis of co-infection was confirmed. The pneumofibrotic changes in the S5 region of the left lung were revealed according to computed tomography. The normalization of aminotransferase activity and bilirubin was noted during dynamic observation. Apparently HAV infection led to a decrease in the immune response, the formation of an insufficient level of neutralizing antibodies in vaccinated against COVID-19 patient M. and contributed to the development of a new coronavirus infection with minimal manifestations in contact with SARS-CoV-2.

1979 ◽  
Vol 9 (1) ◽  
pp. 120-127
Author(s):  
D W Bradley ◽  
H A Fields ◽  
K A McCaustland ◽  
J E Maynard ◽  
R H Decker ◽  
...  

A competitive binding radioimmunoassay (CBA) for antibody to hepatitis A virus (HAV) was evaluated and compared with a standard solid-phase radioimmunoassay for anti-HAV, CBA was found to be sensitive and specific for the detection of anti-HAV, as demonstrated by the 98% concordance of CBA and solid-phase radioimmunoassay test results. The standard CBA test was modified for the differential detection of acute (immunoglobulin M) and convalescent (immunoglobulin G) anti-HAV by incorporation of a step in which immunoglobulin G anti-HAV was preferentially absorbed with S. aureus cells (protein A). The modified CBA test was shown to be capable of differentiating between acute- and convalescent-phase sera. The modified CBAM test was able to detect immunoglobulin M anti-HAV up to approximately 4 weeks after the onset of illness.


mBio ◽  
2016 ◽  
Vol 7 (6) ◽  
Author(s):  
Asuka Hirai-Yuki ◽  
Lucinda Hensley ◽  
Jason K. Whitmire ◽  
Stanley M. Lemon

ABSTRACTHepatitis A virus (HAV) is an unusual picornavirus that is released from cells cloaked in host-derived membranes. These quasi-enveloped virions (eHAV) are the only particle type circulating in blood during infection, whereas only nonenveloped virions are shed in feces. The reason for this is uncertain. Hepatocytes, the only cell type known to support HAV replicationin vivo, are highly polarized epithelial cells with basolateral membranes facing onto hepatic (blood) sinusoids and apical membranes abutting biliary canaliculi from which bile is secreted to the gut. To assess whether eHAV and nonenveloped virus egress from cells via vectorially distinct pathways, we studied infected polarized cultures of Caco-2 and HepG2-N6 cells. Most (>99%) progeny virions were released apically from Caco-2 cells, whereas basolateral (64%) versus apical (36%) release was more balanced with HepG2-N6 cells. Both apically and basolaterally released virions were predominantly enveloped, with no suggestion of differential vectorial release of eHAV versus naked virions. Basolateral to apical transcytosis of either particle type was minimal (<0.02%/h) in HepG2-N6 cells, arguing against this as a mechanism for differences in membrane envelopment of serum versus fecal virus. High concentrations of human bile acids converted eHAV to nonenveloped virions, whereas virus present in bile from HAV-infectedIfnar1−/−Ifngr1−/−andMavs−/−mice banded over a range of densities extending from that of eHAV to that of nonenveloped virions. We conclude that nonenveloped virions shed in feces are derived from eHAV released across the canalicular membrane and stripped of membranes by the detergent action of bile acids within the proximal biliary canaliculus.IMPORTANCEHAV is a hepatotropic, fecally/orally transmitted picornavirus that can cause severe hepatitis in humans. Recent work reveals that it has an unusual life cycle. Virus is found in cell culture supernatant fluids in two mature, infectious forms: one wrapped in membranes (quasi-enveloped) and another that is nonenveloped. Membrane-wrapped virions circulate in blood during acute infection and are resistant to neutralizing antibodies, likely facilitating HAV dissemination within the liver. On the other hand, virus shed in feces is nonenveloped and highly stable, facilitating epidemic spread and transmission to naive hosts. Factors controlling the biogenesis of these two distinct forms of the virus in infected humans are not understood. Here we characterize vectorial release of quasi-enveloped virions from polarized epithelial cell cultures and provide evidence that bile acids strip membranes from eHAV following its secretion into the biliary tract. These results enhance our understanding of the life cycle of this unusual picornavirus.


2012 ◽  
Vol 47 (3) ◽  
pp. 309-312 ◽  
Author(s):  
MZ Amin ◽  
LN Siddique ◽  
MA Slatter ◽  
KK Biswas

Hepatitis A (HAV) infection is caused by the hepatitis A virus which is transmitted through the fecal-oral route. Life long protective antibodies are present after infection. The number of cases of adult hepatitis A has progressively been increasing during the last several decades in Bangladesh. In addition, the pattern of age-specific seroprevalence of anti-HAV has changed with economic growth. The prevalence of anti-HAV in 20-40 year age range has declined rapidly during the last 3 decades. As a result, this age groups has a high risk for HAV infection and clinically overt hepatitis A is increasing in adolescents and adult. The aim of the present study were to assess whether the proportion of adults with acute HAV infection has been increasing over the years and analyze the seroprevalence of immunoglobulin M(IgM) anti- HAV antibodies in young adults below the age of 20 years as well as in cases of chronic liver disease. Sera collected from 530 patients with acute and chronic liver disease attends the Somorita Hospital Ltd. during the previous 2 years and 6 months (Jan. 2008- Jun. 2010) were tested for various serological markers of acute and chronic hepatitis. In addition, 530 normal healthy attendants of the patients above the age of 20 years were tested for IgM anti-HAV as controls. Of 530 patients with acute hepatitis (13.42%) were positive for immunoglobulin M. The patients who were IgM anti-HAV negative were found to be hepatitis B (106 patients), hepatitis C, (10 patients), hepatitis E (150 patients) and unclassified (273 patients). Although the frequency of HAV infection among young adult (< 20 age) had increased (33.33% to 42.35%) in the 2 years and 6 months period, the frequency of HAV infection among adults had also increased (15.38% to 28.13%) during the same period. This study should be helpful for the identification of high risk population for vaccination of hepatitis A. DOI: http://dx.doi.org/10.3329/bjsir.v47i3.13065 Bangladesh J. Sci. Ind. Res. 47(3), 309-312 2012


2018 ◽  
Vol 17 (4) ◽  
pp. 561-568 ◽  
Author(s):  
Mercilena Benjamin ◽  
Shikha Agnihotry ◽  
Anshu Srivastava ◽  
Rishi Bolia ◽  
SK Yachha ◽  
...  

Infection ◽  
1980 ◽  
Vol 8 (6) ◽  
pp. 262-266 ◽  
Author(s):  
M. Roggendorf ◽  
G. Panitz ◽  
R. Scheid ◽  
B. Bayerl ◽  
G. G. Frösner ◽  
...  

2000 ◽  
Vol 74 (23) ◽  
pp. 10950-10957 ◽  
Author(s):  
Andreas Dotzauer ◽  
Ulrike Gebhardt ◽  
Karen Bieback ◽  
Ulrich Göttke ◽  
Anja Kracke ◽  
...  

ABSTRACT The mechanisms underlying the hepatotropism of hepatitis A virus (HAV) and the relapsing courses of HAV infections are unknown. In this report, we show for a mouse hepatocyte model that HAV-specific immunoglobulin A (IgA) mediates infection of hepatocytes with HAV via the asialoglycoprotein receptor, which binds and internalizes IgA molecules. Proof of HAV infection was obtained by detection of HAV minus-strand RNA, which is indicative for virus replication, and quantification of infectious virions. We demonstrate that human hepatocytes also ingest HAV–anti-HAV IgA complexes by the same mechanism, resulting in infection of the cells, by using the HepG2 cell line and primary hepatocytes. The relevance of this surrogate receptor mechanism in HAV pathogenesis lies in the fact that HAV, IgA, and antigen-IgA complexes use the same pathway within the organism, leading from the gastrointestinal tract to the liver via blood and back to the gastrointestinal tract via bile fluid. Therefore, HAV-specific IgA antibodies produced by gastrointestinal mucosa-associated lymphoid tissue may serve as carrier and targeting molecules, enabling and supporting HAV infection of IgA receptor-positive hepatocytes and, in the case of relapsing courses, allowing reinfection of the liver in the presence of otherwise neutralizing antibodies, resulting in exacerbation of liver disease.


1983 ◽  
Vol 14 (6) ◽  
pp. 685-687 ◽  
Author(s):  
Vivian V. Bosch ◽  
Peter C. Dowling ◽  
Stuart D. Cook

1993 ◽  
Vol 31 (5) ◽  
pp. 1299-1302 ◽  
Author(s):  
P L Summers ◽  
D R Dubois ◽  
W H Cohen ◽  
P O Macarthy ◽  
L N Binn ◽  
...  

2013 ◽  
Vol 137 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Adnan Alatoom ◽  
M. Qasim Ansari ◽  
Jennifer Cuthbert

Context.—In the United States, a successful vaccination program for hepatitis A virus (HAV) infection has decreased both its incidence and the true positive rate for diagnostic immunoglobulin M (IgM) antibody to HAV in acute hepatitis. Objective.—To survey positive results of HAV IgM tests and determine the effect of changing ordering options. Design.—We reviewed all positive results for IgM antibody to HAV between January 2007 and December 2010. Patient demographics, clinical history, and laboratory data were recorded and the encounter, order, and reason for test reviewed. Each result was categorized as indicating acute, recent, resolved, or indeterminate HAV infection. Results.—A total of 10 735 tests were performed; 35 patients had 49 positive results. Most positive test results were associated with outpatient visits and were ordered in the assessment of patients with liver disease, but not clinical acute hepatitis. In the final analysis, 4 patients had acute hepatitis A and 20 individual patients had recent and/or resolved hepatitis. All but 1 of the remaining 11 patients had another established cause of liver disease with a positive IgM HAV antibody test result; data to determine causality were insufficient. The total number of tests requested annually decreased more than 35% with the introduction of computerized physician order entry. Conclusions.—Current assays for IgM HAV antibodies are overused in the absence of clinical acute hepatitis; future clinical decision support may improve patterns of order entry. Most patients have findings consistent with HAV exposure but not acute hepatitis; dormant viral infection may be a continuing source of antigen.


Sign in / Sign up

Export Citation Format

Share Document