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Herpes simplex virus type 1 (HSV-1) can establish latent infections in sensory ganglia after primary infection. Subsequent reactivation is usually fatal in immunocompromised patients. We planed to study the effect of immunization in mice with synthetic viral peptides on HSV-1 infection and reactivation. Expression kinetics of gH&gL glycoproteins in cells infected with HSV-1 were also studied using antisera against viral gH and gL peptides. After i.p. immunization with synthetic peptides mimicking various viral glycoproteins,and Rho/45-59 pepeides mimicking anticlotting factor,rhodostomin, BALB/c mice were i.p.challenged with HSV-1 KOS strain. Mice paralysis percentage was recorded and protection efficiency was evaluated. Only gH/561-579 peptide (1 LD50 KOS) and mixed peptides of gH/561-579 and gB/64-78 (100 LD50 KOS) offered significant protection. The binding activity of gH/561- 579 anti-serum to HSV-1 virions was very weak.This suggests that the cellular immunity may be involved in the protective response. The HSV-1 latent infection in BALB/c mice could be established by ocular inoculation with KOS strain. BALB/c mice primed with gH /561-579-OVA conjugate before virus inoculation, eye disease of mice were less severe and virus were detectable in trigeminal ganglia. Priming with gH/561-579 could thus increase the efficiency of latency. Subsequent treatment of latently infected mice with cyclophosphoamide and dexamethasone was able to amply reduce virus titer in trigeminal ganglia, indicating the induction of reactivation is successful. Experiments done by use of "Fluorecent antibody" and "Peroxidase anti-peroxidase" techniques revealed that the expression of gL was earlier than that of gH or virions. gL was detectable 1 hr after infection; but only virions were detectable 4hr later,indicating gH/gL heterodimer were formed and gL antigenicity was thus lost.
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