Human viral encephalitis associated with suid herpesvirus 1

Abstract

Background: Suid herpesvirus type 1 (SHV1) is a type of neurotropic virus able to infect various species. However, the clinical cases of human SHV1 encephalitis are still rarely reported, and the clinical characteristics, treatment, and prognosis of human SHV1 encephalitis are still unclear.

Methods: In this study, we reported 2 cases of human encephalitis associated with SHV1 infection and reviewed the other 18 cases from the literatures. A total of 20 cases with human SHV1 encephalitis were summarized and re-analyzed.

Results: Nineteen of 20 patients had a history of swine-related occupational exposure before illness onset. All patients initially presented with influenza-like symptoms and then developed seizures, disturbed consciousness, and endophthalmitis. All patients with clinical outcome of modified Rankin Scale of 5 or 6 suffered from rapid progressive respiratory failure. The results of cerebrospinal fluid (CSF) indicated aseptic or viral infection. MRI findings of SHV1 encephalitis were prone to distribute in temporal-frontal and insular cortex, which was similar to the pattern of herpes simplex virus encephalitis, while some cases with involvements of gray matter nuclei had a high rate of mortality. Metagenomic next-generation sequencing (mNGS) revealed that all patients had unique SHV1 sequences with variable reads in the CSF.

Conclusions: The variant SHV1 can cause a new type of human viral encephalitis, characterized by acute, fulminating, and catastrophic central nervous system infection. Rapid progressive respiratory failure and extensive lesions of deep gray matter nuclei might be indicators to poor prognosis. No approved treatments for the encephalitis are available, but it is possible to diagnose encephalitis quickly by mNGS.

Keywords: Suid herpesvirus type 1; Pseudorabies virus; Encephalitis; Metagenomic next-generation sequencing.

Fig. 1

Dynamic brain MRI changes in patient 1. MRI on admission revealed high intensities in bilateral temporal lobes on T2 (A) and FLAIR (B) and abnormal intensities in the right insular cortex on T1 (C), T2 (D), and DWI (E). MRI at 1 month after admission showed diffused lesions in bilateral temporal lobes and brain stem on T2 (F); hemorrhagic lesion in occipital lobe on T1 (G); high intensities in temporal-frontal-occipital lobes, thalamus, and basal ganglia on FLAIR (H) and DWI (I); and enhancements on bilateral temporal lobes (J). Arrows indicate the lesions

Fig. 2

Chest CT scan in the 2 patients. No abnormalities on chest CT were found in patient 1 on admission (A and B) and in patient 2 at 3 days after onset (C and D)

Fig. 3

EEG showed generalized slow wave (1–2 Hz delta frequency) diffusely throughout the background in patient 1 (A); paroxysmal spike wave discharge with diffuse slow wave background in patient 2 (B)

Fig. 4

mNGS and PCR validation. mNGS in CSF sample from patient 1 revealed 34 unique reads of SHV1 with 2.43% coverage (A). mNGS in CSF sample from patient 2 found 29 unique reads of SHV1 with 2.55% coverage (B). PCR amplification with a 94 bp product of SHV1 further validated the results of mNGS (C)

Fig. 5

Dynamic brain MRI changes in patient 2. MRI on admission showed high intensities in bilateral temporal lobes (A) and the left insular cortex (B) on T2 and also in bilateral temporal lobes (C) and the left insular cortex (D) on FLAIR. MRI at 10 days after admission showed that the lesions significantly expanded along the temporal-frontal-parietal lobes and thalamus on T2 (E and F) and FLAIR (G and H). Arrows indicate the lesions