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Feline infectious peritonitis (FIP) is caused by infection with the feline coronavirus (FCoV) and is fatal if left untreated. In most cats, FCoV primarily infects the gastrointestinal tract and remains asymptomatic or causes only mild enteritis, with only a small proportion of infected cats developing FIP. An excessive and harmful immune response leading to characteristic (pyo)granulomatous phlebitis is believed to play a key role in the development of FIP, along with complex interactions between host and viral factors. Our research group recently demonstrated successful treatment of cats with naturally occurring FIP using the antiviral nucleoside analogue GS-441524. Treatment led to complete recovery without any relapses for a follow-up period of one year, demonstrating both a short- and long-term cure. To investigate differential gene expression and corresponding molecular pathways in cats with FIP before, during, and after antiviral treatment, RNA sequencing was performed on full blood samples of 18 cats treated successfully in a prospective study. Samples were analyzed before treatment, at different timepoints while on treatment with GS-441524 and after completion of treatment. Additionally, gene expression profiles were compared to 12 healthy FCoV-infected control cats and 5 healthy uninfected control cats. The results revealed both a widespread dysregulation of the blood RNA signature in cats with FIP as well as its rapid normalization within the first week of treatment. Significant changes were already apparent within the first two days of treatment. The results of the present study suggest that elimination of the virus from the blood leads to rapid control and subsequent normalization of the damaging immune response, a finding that corresponds well to the clinical response to treatment. This study illustrates the host response to treatment at the molecular level and provides further evidence that a shorter treatment duration than the 84 days predominantly practiced is sufficient.

Tick-borne encephalitis (TBE) virus is a major cause of central nervous system infections in endemic countries. Here, we present clinical and laboratory characteristics of a large international cohort of patients with confirmed TBE using a uniform clinical protocol. Patients were recruited in eight centers from six European countries between 2010 and 2017. A detailed description of clinical signs and symptoms was recorded. The obtained information enabled a reliable classification in 553 of 555 patients: 207 (37.3%) had meningitis, 273 (49.2%) meningoencephalitis, 15 (2.7%) meningomyelitis, and 58 (10.5%) meningoencephalomyelitis; 41 (7.4%) patients had a peripheral paresis of extremities, 13 (2.3%) a central paresis of extremities, and 25 (4.5%) had single or multiple cranial nerve palsies. Five (0.9%) patients died during acute illness. Outcome at discharge was recorded in 298 patients. Of 176 (59.1%) patients with incomplete recovery, 80 (27%) displayed persisting symptoms or signs without recovery expectation. This study provides further evidence that TBE is a severe disease with a large proportion of patients with incomplete recovery. We suggest monitoring TBE in endemic European countries using a uniform protocol to record the full clinical spectrum of the disease.

Mycoplasma pneumoniae causes atypical pneumonia in children and young adults. Its lack of a cell wall makes it resistant to beta-lactams, which are the first-line treatment for typical pneumonia. Current diagnostic tests are time-consuming and have low specificity, leading clinicians to administer empirical antibiotics. Using a LASSO regression simulation approach and blood microarray data from 107 children with pneumonia (including 30  M. pneumoniae ) we identify eight different transcriptomic signatures, ranging from 3-10 transcripts, that differentiate mycoplasma pneumonia from other bacterial/viral pneumonias with high accuracy (AUC: 0.84–0.95). Additionally, we demonstrate that existing signatures for broadly distinguishing viral/bacterial infections and viral/bacterial pneumonias are ineffective in distinguishing M. pneumoniae from viral pneumonia. The new signatures are successfully validated in an independent RNAseq cohort of children with pneumonia, demonstrating their robustness. The high sensibility of these signatures presents a valuable opportunity to guide the treatment and management of M. pneumoniae pneumonia patients. Using blood microarray data from 107 children with pneumonia, the authors here identify eight transcriptomic signatures that distinguish Mycoplasma pneumoniae pneumonia from other viral and bacterial pneumonias, paving the way for precise diagnosis and targeted treatment guidance.