Study: SARS-CoV-2 Infection Causes Hyperglycemia in Cats. Image Credit: Khon Thai Phap / Shutterstock

SARS-CoV-2 can cause hyperglycemia in cats

In a recently published study Journal of Infectious DiseasesResearchers investigated the relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and hyperglycemia in cats.

The exact mechanisms underlying the emergence of new-onset diabetes among patients with coronavirus disease 2019 (COVID-19) are unknown; however, it is likely due to several complex and interrelated etiologies such as impaired glucose utilization, stress hyperglycemia, steroid-induced diabetes, and pre-admission diabetes as well as insulin secretion. In addition, previous research has shown that SARS-CoV-2 causes transient hyperglycemia and decreased pancreatic ß-cell function in the context of epidemic-induced pneumonia.

Studies: SARS-CoV-2 Infection Causes Hyperglycemia in Cats. Image Credit: Khon Thai Phap / Shutterstock

about the study

This study presented a comprehensive analysis of hyperglycemia associated with SARS-CoV-2 infection in domestic cats.

To investigate the replication and pathogenesis of SARS-CoV-2 in cats, nine cats aged 70 to 100 days were categorized as infection and control cohorts. 2×10 to cats in the infection cohort7 TCID50/mL of strain HB-01. Using the same techniques, supernatant of Vero E6 cell culture was used to simulate infection in control cats. The subjects’ clinical signs were then observed for seven days. On the third, fifth, and seventh day after infection, two infected cats and one mock-infected cat were euthanized to allow collection of samples.

The team tested the cats’ blood sugar levels before and after viral infection to determine if SARS-CoV-2 affects glucose metabolism. Immunohistochemistry triple-labeling for viral nucleocapsid protein (NP), insulin, and glucagon was also performed. To confirm whether SARS-CoV-2 causes hyperglycemia in cats, a vaccine-preserving experiment was performed. Six cats were vaccinated three times with inactivated SARS-CoV-2. Three cats were immunized under the same conditions as the culture medium as a control.


At three, five, and seven days after infection (dpi), viral ribonucleic acid (RNA) was detected in the turbinates, bronchi, trachea, and entire lung lobes of infected cats. The burden of viral RNA in the lung tissue was relatively less than that of the upper respiratory tract. Notably, pancreatic tissues from all infected cats gave viral RNA-positive results at five and seven dpi. However, liver, kidney, spleen, heart tissues and testicular tests were negative. Measurement of viral titers showed that infectious viruses proliferated in the turbinates, lung tissues, and trachea, but not in the liver, heart, small intestine, spleen, pancreas, brain, kidneys, and submaxillary lymph nodes.

The vast majority of cats infected with SARS-CoV-2 exhibited hyperglycemia, but none of the subjects in the control group did. This showed a link between COVID-19 and blood glucose levels. Microscopic examination and anatomical features revealed that COVID-19 did not cause any visible pathological changes in the cat pancreas. Also, the islets were easily visible without detecting any abnormal or diseased cells. Furthermore, immunohistochemical labeling revealed the presence of SARS-CoV-2 NP among pancreatic islet cells of infected cats. SARS-CoV-2 NP was specifically found in the turbinates, tracheas, soft palates, bronchioles, and alveolar epithelial cells of infected cats. However, no NPs were found in liver, kidney, or brain tissue samples.

The team found a few viral NP-glucagon double positive cells, with only a small number of viral NP-insulin double positive cells. Similarly, the same results were recorded when antibodies specific to the SARS-CoV-2 spike protein were used. In addition, triple immunohistochemical staining for angiotensin converting enzyme-2 (ACE-2), viral NP and glucagon revealed abundant triple positive cells. There was no SARS-CoV-2 NP immunopositivity in pancreatic tissue isolated from uninfected cats. Infected cats with a high burden of SARS-CoV-2 are susceptible to pancreatic SARS-CoV-2 infection, as are infection of endocrine and exocrine cells.

After three rounds of vaccination with inactivated SARS-CoV-2, the serum neutralizing antibody titer in vaccinated cats reached 1:640. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) data showed that vaccinated cats had a lower viral load than control animals. In addition, SARS-CoV-2 nucleic acid was not detected in the pancreatic tissue of vaccinated cats. Similarly, post-immunization blood sugar levels of vaccinated cats did not show any significant change. On the other hand, control subjects’ blood sugar levels rose significantly. SARS-CoV-2 infection most likely caused an increase in blood sugar levels in affected cats.


The study findings showed an unexpected and atypical increase in blood sugar levels in cats infected with SARS-CoV-2 under laboratory conditions. SARS-CoV-2 protein and RNA were also found in the pancreas of these cats. The team also highlighted the cellular localization pattern exhibited by SARS-CoV-2 among pancreatic endocrine cells.

Journal reference:

  • Yufei Zhang, Jindong Gao, Kun Huang, Ya Zhao, Xianfeng Hui, Ting Wang, Changmin Hu, Xiaomei Sun, Ying Yang, Chao Wu, Xi Chen, Zhong Zou, Lian zong Zhao, Meilin Jin, SARS-CoV-2 Causes of Infection Hyperglycemia in Cats, Journal of Infectious Diseases, Vol 226, Issue 9, 1 November 2022, Pages 1568–1576, DOI:

#SARSCoV2 #hyperglycemia #cats

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