The major limitation of the study is that the diagnosis sCJD was not confirmed by autopsy. Clinical diagnostic criteria of sCJD include a combination of characteristic neuropsychiatric symptoms and signs, elevated cerebrospinal fluid (CSF) proteins 14-3-3, high CSF tau protein, EEG, MRI, and real-time quaking-induced conversion (RT-QuIC) [2], but the definite diagnosis is made by autopsy. The sensitivity and specificity of the tests used do not exceed 92% and 95%, respectively [3].

A second limitation of the study is that the CSF was not tested for SARS-CoV-2 by PCR. A negative nasopharyngeal swab test does not rule out cerebral SARS-CoV-2 infection. A negative PCR for SARS-CoV-2 in the CSF would have ruled out infectious SARS-CoV-2 encephalitis. Immune encephalitis caused by SARS-CoV-2 infection could have been excluded by the absence of antibodies associated with immune encephalitis and normal CSF levels of cytokine, chemokines, and glial factors.

We disagree with the statement that there was a rapid deterioration as the patient died 4 months after the disease onset [1]. The average duration of symptoms in patients with sCJD is 4 months of disease duration [4], so there is no acceleration or worsening of neurological deterioration or shortened survival. At the same time, the study design (case report) is not suitable for the conclusion that when a sCJD patient is infected with SARS-CoV-2, neurological decline is accelerated, worsened and, consequently, overall survival is shortened [1]. From a single patient and the lack of a control group, such conclusions remain unsupported. Whether SARS-CoV-2 infection actually worsens and accelerates that sCJD needs to be investigated by a multicentre design in patients with autopsy-confirmed sCJD.