First case of postmortem study in a patient vaccinated against SARS-CoV-2

Author:TorstenHansenaUlfTitzeaNidhi Su AnnKulamadayil-HeidenreichbSabineGlombitzacJohannes, et. al.


• We report on a patient with a single dose of vaccine against SARS-CoV-2.

• He developed relevant serum titer levels but died 4 weeks later.

• By postmortem molecular mapping, we found viral RNA in nearly all organs examined.

• However, we did not observe any characteristic morphological features of COVID-19.

Immunogenicity might be elicited, while sterile immunity was not established.


A previously symptomless 86-year-old man received the first dose of the BNT162b2 mRNA COVID-19 vaccine. He died 4 weeks later from acute renal and respiratory failure. Although he did not present with any COVID-19-specific symptoms, he tested positive for SARS-CoV-2 before he died. Spike protein (S1) antigen-binding showed significant levels for immunoglobulin (Ig) G, while nucleocapsid IgG/IgM was not elicited. Acute bronchopneumonia and tubular failure were assigned as the cause of death at autopsy; however, we did not observe any characteristic morphological features of COVID-19. Postmortem molecular mapping by real-time polymerase chain reaction revealed relevant SARS-CoV-2 cycle threshold values in all organs examined (oropharynx, olfactory mucosa, trachea, lungs, heart, kidney and cerebrum) except for the liver and olfactory bulb. These results might suggest that the first vaccination induces immunogenicity but not sterile immunity.



We report on an 86-year-old male resident of a retirement home who received vaccine against SARS-CoV-2. Past medical history included systemic arterial hypertensionchronic venous insufficiencydementia and prostate carcinoma. On January 9, 2021, the man received lipid nanoparticle-formulated, nucleoside-modified RNA vaccine BNT162b2 in a 30 μg dose. On that day and in the following 2 weeks, he presented with no clinical symptoms (Table 1). On day 18, he was admitted to hospital for worsening diarrhea. Since he did not present with any clinical signs of COVID-19, isolation in a specific setting did not occur. Laboratory testing revealed hypochromic anemia and increased creatinine serum levels. Antigen test and polymerase chain reaction (PCR) for SARS-CoV-2 were negative.

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The Severe Acute Respiratory Syndrome

Authors: Joseph S.M. Peiris, M.D., D.Phil., Kwok Y. Yuen, M.D., Albert D.M.E. Osterhaus, Ph.D., and Klaus Stöhr, Ph.D.

The severe acute respiratory syndrome (SARS) is responsible for the first pandemic of the 21st century. Within months after its emergence in Guangdong Province in mainland China, it had affected more than 8000 patients and caused 774 deaths in 26 countries on five continents. It illustrated dramatically the potential of air travel and globalization for the dissemination of an emerging infectious disease and highlighted the need for a coordinated global response to contain such disease threats. We review the cause, epidemiology, and clinical features of the disease.


An unusual atypical pneumonia emerged in Foshan, Guangdong Province, mainland China, in November 2002.1,2 In February and March 2003, the disease spread to Hong Kong and then to Vietnam, Singapore, Canada, and elsewhere (Table 1).3,4 The new disease was named the severe acute respiratory syndrome (SARS), and a preliminary case definition was established.4 A novel coronavirus (SARS-CoV) was identified as the causative agent.5-10 Coronaviruses are a family of enveloped, single-stranded–RNA viruses causing disease in humans and animals, but the other known coronaviruses that affect humans cause only the common cold.

The presence of SARS-CoV has been demonstrated by reverse-trancriptase polymerase chain reaction (RT-PCR) and the isolation of the virus from respiratory secretions, feces, urine, and tissue specimens from lung biopsy,11,12 indicating that the infection is not confined to the respiratory tract. The experimental infection of cynomolgus macaques with SARS-CoV produced a pneumonia that was pathologically similar to SARS in humans.8,9 Other pathogens, including human metapneumovirus13,14 and chlamydia,7,15 have been detected together with SARS-CoV in some patients with SARS, but they have not been found consistently.5,9 The experimental infection of macaques with human metapneumovirus did not lead to a SARS-like disease, and coinfection of macaques with human metapneumovirus and SARS-CoV did not enhance the pathogenicity of the SARS-CoV in this animal model.8 Thus, all the information that is available to date suggests that SARS-CoV is necessary and sufficient for the causation of SARS in humans, but it remains to be determined whether microbial or other cofactors enhance the severity or transmissibility of the disease. The complete genetic sequence of the SARS-CoV genome was determined, and it provided confirmation that SARS-CoV belongs to a new group within the coronavirus family.

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