Canine herpesvirus

Canine herpesvirus (CHV) is a virus that infects only dogs and can lead to reproductive disorders in female dogs, such as infertility, miscarriage, and stillbirths, as well as penile and preputial inflammation in male dogs. In newborn puppies, it often causes fatal infections resulting in death. This virus was first identified and isolated as early as 1965. Although the newly issued Chinese standard for Microbiological and Parasitological Classification and Monitoring of Laboratory Animals (GB 14922-2022) does not explicitly address this virus, reports indicate that CHV is widespread among both domestic and wild dogs worldwide. Serological surveys conducted in Europe and North America have revealed that the prevalence of this virus remains alarmingly high in these regions. Once an outbreak occurs, CHV can inflict severe economic losses on dog breeding facilities and research laboratories working with experimental animals.

Canine herpesvirus is a double-stranded DNA virus belonging to the Alphaherpesvirinae subfamily within the Varicellovirus genus of the Herpesviridae family. It can infect and replicate in mucosal epithelial cells and lymphoid tissues. Like other herpesviruses, after initial infection, it enters a latent state, persisting in trigeminal or lumbosacral ganglia, as well as in the tonsils, parotid salivary glands, nasopharynx, gastric lymph nodes, and pulmonary lymphoid tissues. Under external influences such as age, pregnancy, environmental stress, immunosuppressive treatments, and co-infections with other pathogens, the virus can reactivate, leading to clinical disease in animals, facilitating transmission, and maintaining persistent circulation within dog populations. The virus is sensitive to lipid solvents and can be rapidly inactivated by common disinfectants; it is also quickly destroyed at temperatures above 40°C. Notably, the virus replicates most efficiently at 36°C. This virus has only one serotype and can only multiply in canine cells—specifically, it replicates most rapidly in canine kidney cells. Interestingly, the virus exhibits very low immunogenicity: following infection, neutralizing antibody levels rise significantly and remain relatively high for up to two months. Low-titer antibodies, however, can persist for at least two years. Serum antibodies play a crucial role in pregnant females by suppressing viremia and preventing fetal infection via transplacental transmission. Moreover, the immune status of the mother dog is critical not only for protecting her own health but also for ensuring the survival of infected puppies.

CHV spreads directly through bodily fluids, including oral, nasal, and genital secretions, as well as urine. It can also be transmitted vertically via the reproductive tract. Puppies younger than 3 weeks old, due to their immature immune systems and weak resistance, often develop acute symptoms after CHV infection, typically leading to death within a few days to one week—with mortality rates reaching as high as 100%. In contrast, puppies older than 3 weeks and adult dogs usually remain asymptomatic, while older dogs infected with CHV often exhibit only mild respiratory signs. Serological surveys reveal that, in the absence of vaccination, antibody-positive rates among household dogs and group-housed dogs are as follows: 88% in the UK, 80%–85.5% in Norway, 45.8% in Belgium, 39.3% in the Netherlands, 27.9% in Italy, and just 6% in the United States. Notably, pet dogs show a much lower antibody positivity rate—only 3.1%. Meanwhile, larger-scale kennels tend to have higher seropositivity rates, particularly when kennel conditions are poor or when there is a history of kennel cough within the facility. According to a study reported in the literature, dogs initially testing seronegative eventually showed seroconversion upon repeated antibody testing after several breeding cycles. This suggests that the true prevalence of CHV in kennels may be even higher, potentially affecting the entire dog population. Moreover, chronically infected dogs may intermittently shed the virus at unpredictable intervals over months or even years.

Diagnosis of CHV infection can be achieved by isolating and culturing the virus in viral cell lines; however, this method is time-consuming, and according to existing literature, the virus is notoriously difficult to isolate—whether during its latent infection phase or active shedding period. While PCR is more sensitive than virus culture, under natural conditions where CHV is prevalent and immunity is present, viral shedding may be transient, lasting only a few days. Therefore, it is recommended to collect samples from dogs over several consecutive days. Additionally, PCR analysis for diagnostic purposes should be conducted at specific times—such as when reproductive disorders or genital lesions occur. If no clinical symptoms are observed, PCR testing is not advised for definitive diagnosis. On the other hand, the ELISA method within serological approaches can effectively monitor the prevalence of CHV-specific antibodies within a population, helping determine whether individuals have been previously infected with the virus. In vaccinated groups, ELISA can also be used to assess vaccine efficacy. However, when performing ELISA tests on populations that have never received vaccination, repeated testing is essential, as periodic viral shedding in dogs can lead to fluctuations in antibody titers. A single-point measurement at one specific time may fail to accurately reflect the animal’s true infection status.

CHV is a common infection; although some kennels may remain virus-free, positive kennels often exhibit a high seroprevalence, with a significant portion of the dog population showing high-titer antibodies. The clinical and subclinical carriage of the virus is complex and challenging to distinguish. Moreover, antibody titers in the body can fluctuate depending on the estrous cycle as well as potential external factors. Even seronegative pregnant bitches exposed in virus-endemic kennels—and particularly those newly introduced to such facilities carrying latent infections—can inadvertently bring the virus into the kennel, leading to severe reproductive issues in seronegative pregnant females. Therefore, it is recommended that breeding females in both virus-free and historically troubled kennels undergo vaccination as part of proactive management strategies.

Dog breeding and sales facilities should immediately isolate any suspected sick dogs while simultaneously carrying out thorough disinfection. Dead or diseased dog carcasses must be deeply buried and incinerated to prevent the spread and escalation of the outbreak. As there is no specific cure for this disease, proactive vaccination efforts are essential for preventive management.

References

1. Decaro N, Martella V, Buonavoglia C. Canine adenoviruses and herpesvirus. Vet Clin North Am Small Anim Pract. 2008 Jul;38(4):799-814

2. Ronsse V, Verstegen J, Thiry E, Onclin K, Aeberlé C, Brunet S, Poulet H. Canine Herpesvirus-1 (CHV-1): Clinical, Serological, and Virological Patterns in Breeding Colonies. Theriogenology. 2005 Jul 1;64(1):61-74.

3. Rota A, Dogliero A, Biosa T, Messina M, Pregel P, Masoero L. Seroprevalence of Canine Herpesvirus-1 in Breeding Dogs with or Without Vaccination in Northwest Italy. Animals (Basel). 2020 Jun 29;10(7):1116.

4. Clinical Small Animal Internal Medicine, This edition first published 2020 by John Wiley & Sons, Inc

5. Isolation and Identification of Canine Herpesvirus, along with Bioinformatics Analysis of the US6 Gene