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Deer Tick Virus (DTV) is an animal derived virus that naturally hosts North American deer mice. This virus, along with Borrelia burgdorferi and the novel Hantavirus, constitutes the main pathogen combination carried by deer mice. A study published in the journal Nature Communications in 2021 confirmed that as hosts of various zoonotic pathogens, deer and mouse populations carry a pathogen lineage that includes deer tick viruses, and their biological associations have been validated through scientific experiments.
Figure 1. Deer tick virus (DTV) in humans and mice. (Ebel, Gregory D.,et al, 2010)
The North American deer mouse (Peromyscus maniculatus) has been confirmed as a natural host of deer tick virus, and this rodent is distributed in temperate forest ecosystems in North America. The virus spreads through tick species in the family Ixodidae (mainly shoulder tick), forming an ecological cycle chain of "host vector host" In 2021, a Canadian research team confirmed through molecular biology testing that the carrier rate of deer tick virus in wild deer and mouse populations remained in the range of 5-15% for a long time. After completing replication in tick midgut epithelial cells, the virus spreads to new hosts through salivary glands.
DTV has a single stranded sense RNA genome of approximately 11 kb in length, encoding a polyprotein that is cleaved into three structural proteins (capsid C, pre membrane prM, and envelope E) and seven non structural proteins (NS). Phylogenetic analysis of the E gene and other genomic regions confirms that DTV is an independent lineage within the POWV species, with over 90% amino acid homology to the prototype POWV lineage. The main vectors of transmission are black legged ticks and scapular ticks, which are transmitted to humans through bites from infected ticks. The geographical range of digital television is consistent with the geographical range of its vectors, mainly in the northeastern and central northern parts of the United States. Although human infection is rare, it is considered to be serious. Because of nonspecific or asymptomatic infection, the incidence rate may be underestimated.
The pathogenesis of DTV follows a common pattern of neurotropic yellow virus. After inoculation through tick bites, the initial virus replication is believed to occur in local dendritic cells and macrophages, leading to viremia and subsequent nerve invasion. The infection cycle begins when the viral E protein binds to unknown receptors on susceptible cells, such as dendritic cells in the skin. The virus is internalized through endocytosis, and the acidic environment of the endosome triggers E protein mediated fusion, releasing the viral genome into the cytoplasm. The viral RNA is translated and the NS3-NS2B protease cleaves the polyprotein. The replication complex, including NS5 and NS3, assembles on the endoplasmic reticulum membrane to generate a new viral RNA genome. Meanwhile, NS5 blocks the host's interferon response by interfering with the STAT1/STAT2 signaling pathway, thereby weakening the antiviral state.
Human DTV infection ranges from asymptomatic to severe neuroinvasive diseases. After a incubation period of one week to one month, the initial symptoms may include fever, headache, vomiting, and weakness. This may rapidly develop into encephalitis or meningitis, manifested as confusion, loss of coordination, difficulty speaking, seizures, and paralysis. The mortality rate is about 10-15%, and about half of the survivors experience long-term neurological deficits such as recurrent headaches, muscle atrophy, and memory problems.
The diagnosis of DTV infection is based on clinical suspicion and laboratory testing of potential tick contact patients in endemic areas.
| Diagnosis | Details |
| Molecular Method | Reverse transcription polymerase chain reaction (RT-PCR) can detect viral RNA in acute phase serum or cerebrospinal fluid (CSF). |
| Serological Methods | Use detection methods such as ELISA and PRNT to detect virus specific IgM and neutralizing antibodies in serum or CSF. Recombinant E protein is particularly valuable in these immunoassays due to its specificity. |
The deer tick virus is a serious threat in areas where its tick vector is established, although it is rare. It is classified as the genotype of Powassan virus, highlighting its close relationship with known human pathogens. The molecular pathogenesis of DTV involves the synergistic effect of viral proteins, such as the entering E protein and the immune escape NS5 protein, particularly in blocking the interferon signaling pathway. These interactions promote viral replication and neural invasion, leading to potentially catastrophic encephalitis. With the help of tools such as recombinant viral proteins, it is crucial to continue studying their specific host interactions and developing strategies to improve diagnosis, understand disease mechanisms, and ultimately prevent this serious infection.
Reference
| Target | Cat. No. | Product Name | Host | |
| POWV | DAG-WT5844 | Recombinant Deer tick virus Envelope protein [His] | HEK293 cells | Inquiry |
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