Hans Lutz

Hans Lutz

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Hans Lutz

Clinical Laboratory, Department of Clinical Diagnostics and Services and Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, CH 8057 Zurich, Switzerland

Research Focus & Metrics

Academic Career Length

12Years (2015-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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24 July 2020 in Pathogens
Verified
Journal Article
Open access
PDF file
MLMirjam Lutz
Mirjam Lutz
ASAline Steiner
Aline Steiner
VCValentino Cattori
Valentino Cattori
Regina Hofmann-LehmannRegina Hofmann-Lehmann
Regina Hofmann-Lehmann
HLHans Lutz
Hans Lutz
MMMarina L. Meli
Marina L. Meli
Feline Infectious Peritonitis (FIP)—the deadliest infectious disease of young cats in shelters or catteries—is induced by highly virulent feline coronaviruses (FCoVs) emerging in infected hosts after mutations of less virulent FCoVs. Previous studies have shown that some mutations in the open reading frames (ORF) 3c and 7b and the spike (S) gene have implications for the development of FIP, but mainly indirectly, likely also due to their association with systemic spread. The aim of the present study was to determine whether FCoV detected in organs of experimentally FCoV infected healthy cats carry some of these mutations. Viral RNA isolated from different tissues of seven asymptomatic cats infected with the field strains FCoV Zu1 or FCoV Zu3 was sequenced. Deletions in the 3c gene and mutations in the 7b and S genes that have been shown to have implications for the development of FIP were not detected, suggesting that these are not essential for systemic viral dissemination. However, deletions and single nucleotide polymorphisms leading to truncations were detected in all nonstructural proteins. These were found across all analyzed ORFs, but with significantly higher frequency in ORF 7b than ORF 3a. Additionally, a previously unknown homologous recombination site was detected in FCoV Zu1.

22 June 2015 in Journal of Feline Medicine and Surgery
Verified
Journal Article
Closed access
HLHans Lutz
Hans Lutz
DADiane D Addie
Diane D Addie
CBCorine Boucraut-Baralon
Corine Boucraut-Baralon
HEHerman Egberink
Herman Egberink
TFTadeusz Frymus
Tadeusz Frymus
EDEuropean Advisory Board On Cat Diseases
European Advisory Board On Cat Diseases
Overview: Borna disease virus (BDV) has a broad host range, affecting primarily horses and sheep, but also cattle, ostriches, cats and dogs. In cats, BDV may cause a non-suppurative meningoencephalomyelitis (‘staggering disease’). Infection: The mode of transmission is not completely elucidated. Direct and indirect virus transmission is postulated, but BDV is not readily transmitted between cats. Vectors such as ticks may play a role and shrews have been identified as a potential reservoir host. Access to forested areas has been reported to be an important risk factor for staggering disease. Disease signs: It is postulated that BDV may infect nerve endings in the oropharynx and spread via olfactory nerve cells to the central nervous sytem. A strong T-cell response may contribute to the development of clinical disease. Affected cats develop gait disturbances, ataxia, pain in the lower back and behavioural changes. Diagnosis: For diagnostic purposes, detection of viral RNA by reverse transcription PCR in samples collected from cats with clinical signs of Borna disease can be considered diagnostic. Serology is of little value; cats without signs of Borna disease may be seropositive and yet not every cat with BDV infection has detectable levels of antibodies. Human infection: A hypothesis that BDV infection may be involved in the development of selected neurological disorders in man could not be confirmed. A research group within the German Robert Koch Institute studied the potential health threat of BDV to humans and concluded that BDV was not involved in the aetiology of human psychiatric diseases.

12 June 2020 in Viruses
Verified
Journal Article
Open access
PDF file
FFFilippo Ferri
Filippo Ferri
FPFederico Porporato
Federico Porporato
FRFrancesco Rossi
Francesco Rossi
DEDaniela Enache
Daniela Enache
CCCarolina Callegari
Carolina Callegari
EZEric Zini
Eric Zini
Feline parvovirus (FPV) causes severe gastroenteritis and leukopenia in cats; the outcome is poor. Information regarding specific treatments is lacking. Class A CpG oligodeoxynucleotides (CpG-A) are short single-stranded DNAs, stimulating type I interferon production. In cats, CpG-A induced an antiviral response in vivo and inhibited FPV replication in vitro. The aim was to prospectively investigate the effects of CpG-A on survival, clinical score, hematological findings, antiviral response (cytokines), viremia, and fecal shedding (real-time qPCR) in cats naturally infected with FPV. Forty-two FPV-infected cats were randomized to receive 100 µg/kg of CpG-A (n = 22) or placebo (n = 20) subcutaneously, on admission and after 48 h. Blood and fecal samples were collected on admission, after 1, 3, and 7 days. All 22 cats showed short duration pain during CpG-A injections. The survival rate, clinical score, leukocyte and erythrocyte counts, viremia, and fecal shedding at any time-point did not differ between cats treated with CpG-A (50%) and placebo (40%). Antiviral myxovirus resistance (Mx) gene transcription increased in both groups from day 1 to 3 (p = 0.005). Antibodies against FPV on admission were associated with survival in cats (p = 0.002). In conclusion, CpG-A treatment did not improve the outcome in cats with FPV infection. FPV infection produced an antiviral response.