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Review
. 2023 Nov 16:14:1281384.
doi: 10.3389/fimmu.2023.1281384. eCollection 2023.

Towards a comprehensive view of the herpes B virus

Jiangling Lu #  1   2   3 , Yiru Long #  1   2 , Jianhua Sun  1   2   3 , Likun Gong  1   2   3
Affiliations
Review

Towards a comprehensive view of the herpes B virus

Jiangling Lu et al. Front Immunol. .

Abstract

Herpes B virus is a biosafety level 4 pathogen and widespread in its natural host species, macaques. Although most infected monkeys show asymptomatic or mild symptoms, human infections with this virus can cause serious neurological symptoms or fatal encephalomyelitis with a high mortality rate. Herpes B virus can be latent in the sensory ganglia of monkeys and humans, often leading to missed diagnoses. Furthermore, the herpes B virus has extensive antigen crossover with HSV, SA8, and HVP-2, causing false-positive results frequently. Timely diagnosis, along with methods with sensitivity and specificity, are urgent for research on the herpes B virus. The lack of a clear understanding of the host invasion and life cycle of the herpes B virus has led to slow progress in the development of effective vaccines and drugs. This review discusses the research progress and problems of the epidemiology of herpes B virus, detection methods and therapy, hoping to inspire further investigation into important factors associated with transmission of herpes B virus in macaques and humans, and arouse the development of effective vaccines or drugs, to promote the establishment of specific pathogen-free (SPF) monkeys and protect humans to effectively avoid herpes B virus infection.

Keywords: diagnosis; herpes B virus; therapy; zoonotic pathogens; α-herpesvirus.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Herpes B virus genome organization, genotypes, and virion structure model. (A) Genome structure of the B virus. The structural organization of the B virus genome, shows the long unique region (UL) and the short unique region (US), each bounded by an inverted internal repeat region (TRL, IRL, TRS, and IRS). The location of several functional genes (ICP0, ICP4, ICP22, ICP27 and ICP47) that impact gene expression and replication, and other genes (ul1, ul10, ul22, ul27, ul44, ul53 and US4-8) that produce envelope glycoprotein, are indicated. (B) Genotypes of the B virus. Sequence variation on BV isolates from different macaque species confirmed the existence of different genotypes of the B virus. These isolates from rhesus macaques (BVrh), cynomolgus macaques (BVcy), pig-tailed macaques (BVpt), lion-tailed macaques (BVlt) were completely sequenced, except for Janpanese macaques (BVjp). The complete genomes of these isolates have been sequenced, except for mfu#17. (C) Herpes B virus structure model.
Figure 2
Figure 2
Comparison of the amino acid sequences of the gB (A) and gD (B) between B virus (E2490)and HSV (HSV-1 and HSV-2). Red box, white character: strict identity. Red character: similarity in a group. Blue frame: similarity across groups.
Figure 3
Figure 3
Model of the B virus and HSV entry mechanisms. α-herpesvirus shared entry strategies into host cells. (A) HSV-1 and HSV-2 fuse with a host cell at the cell membrane. The gD dimer (red), gH-gL heterodimer (dark and light blue), and gB trimer (green) are necessary and sufficient for entry. gD binds to several entry receptors (small arrow), including HVEM (purple), Nectin-1 (yellow), Nectin-2 (grey), and 3-OST HS (light green). The binding of gD to its corresponding receptor transmits a signal to gH-gL (light grey arrow), which activates the fusion protein gB (light grey arrow) to undergo a conformational change. (B) As gB refolds into its postfusion conformation, the merging of membranes forms a fusion pore through which the viral content can enter the host cells. (C) The entry mechanisms of the B virus and HSV are similar but not identical. B virus can effectively use both Nectin-1 and Nectin-2 as cellular receptors for entry into human cells but not the HVEM-mediated entry pathway (red fork). B virus utilizes 3-OST HS to bind gD, which is unknown (red question mark). PILRα, an HSV-1 gB fusion receptor, and did not function as an entry receptor (red fork). Exactly how B viruses achieve membrane fusion (red question mark) still needs to be studied more systematically and deeply.
Figure 4
Figure 4
Diagnosis of the B virus. Vero cells were inoculated with swab samples obtained from the oral, conjunctiva, wound (bites and scratches), and genital epithelium, examined for CPE by plaque assay. The swab samples can also be tested for the B virus DNA by PCR tests. Herpes B virus antigen, alternative laboratory antigen, and monoclonal antibodies (mAbs) were used to coat wells of a polystyrene plate to detect anti-B virus antibodies by using ELISAs.
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Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by Foundation of Shanghai Science and Technology Committee (No. 22140900501).