Herpes simplex virus (HSV-1) is a virus which produces both lytic and latent infection. In the latter case it persists in a quiescent form in the neural ganglia for the lifetime of its host.

My question is whether the antibodies raised against the virus persist for the lifetime of the individual.

I understand that exposure to the virus again would activate the memory B cells and lead to the elicitation of these antibodies. But in general, what is the scenario with the circulating antibodies?

I found some websites stating that the antibodies persist for the lifetime of the individual, but I could not find any research publications to support this.

  • $\begingroup$ @MattDMo Thank you for your response. After the 3-4 weeks, the level of antibodies will deplete unless there is a reinfection. However, it is known that plasma cells residing in bone marrow can secrete antibodies for a long time even after the clearance of the virus. Not sure if it applies to herpes virus infection as well. $\endgroup$
    – Riq
    Feb 16, 2022 at 17:27
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    $\begingroup$ Which Herpesvirus are you talking about? Human Herpes Virus Type 1 (HSV1) or what? Until you tell us, nobody can answer your question, and anyone who has has made the same mistake as you. $\endgroup$
    – David
    Feb 16, 2022 at 19:40
  • $\begingroup$ @David I guess it does not matter as all herpes virus remain in our body for the rest of our life after infection. However, to be specific HSV-1 can be used. $\endgroup$
    – Riq
    Feb 18, 2022 at 0:03
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    $\begingroup$ Human herpesviruses range from alpha (HSV1 and 2, varicella zoster), beta (cytomegalovirus) to gamma (Epstein-Barr virus). So I think scientifically it is best to specify. I have edited your question accordingly. It would be helpful if you could give links to the sites you quote as saying that antibodies stay a lifetime. $\endgroup$
    – David
    Feb 18, 2022 at 8:48

1 Answer 1


For the vast majority of a herpesvirus infection, the virus genome is only present in the nucleus of latently-infected neuronal cells; there are no virus particles in the body. My understanding is that there will therefore be no circulating antibodies unless the latently infected neurons reactivate and begin producing viral particles. However, in this 2005 review, "Immunity in latent Herpes simplex virus infection", mouse studies found that infected neurons had CD8+T cells stuck to them that stayed there and secreted interferons for the lifetime of the animal:

In mice, CD8+T cells invade TG ~7 days after HSV-1 infection, reach maximum ~4 days p.i. and are then retained in a significant number seemingly for the life-time of the animal. Significantly, HSV-1-specific CD8+T cells are persistently stimulated within the latently infected TG. ... The steady expression of IFN-γ and TNF-α in latently infected TG suggests continuous stimulation of the cells producing these cytokines. Expression of these cytokines is tightly regulated and subsides within two hours of withdrawal of the stimulant. Since IFN-γ can block HSV-1 reactivation from latency in sensory neurons, such a CD8+T cell population is ideally suited to the function of long-term protection with minimal tissue destruction (Kodukula et al., 1999; Liu et al., 2000, 2001; Mueller et al., 2003; Stuart et al., 2004).

So this implies it's the presence of T-cells in the trigeminal ganglion (TG in the above quote) that keeps infected neurons from reactivating and producing new virus. Since the T-cells are apparently being continuously stimulated, it seems possible that B-cells could also be getting stimulated and secrete antibodies, but I haven't seen that possibility addressed anywhere. Also, this continuous stimulation of the immune cells may only happen in mice, not in human infections:

In contrast to latently HSV-1-infected mice, the frequent reactivation of HSV-1 in human TG may reflect a less efficient CD8+T cell recognition. This would be compatible with the fact that HSV-1 ICP47 protein inhibits TAP-mediated transport of antigenic peptides more efficiently in human than in mouse cells.

Mice with suppressed B-cells were not found to be less effective at preventing reactivation of latent HSV-1 infections.

Finally, the viral antigen that most of the reactivation-inhibiting T-cells were found to be going after was a fragment of gB, an envelope glycoprotein somewhat similar to the famous coronavirus spike protein. I would expect this antigen to also be a major target for antibodies.

  • $\begingroup$ Thank you for your response. Here is the a publication: dx.doi.org/10.1128/mBio.00678-17 Like T cells in trigeminal ganglion (TG) gets stimulated, the antibodies also increases after infection and persisted 8 months after infection (latest time studied). IgG concentrations were significantly increased in the TG and brain but not in the lung or liver. They persisted for long in human and murine TG. The data in the paper shows that TG IgG originates both from locally antibody-secreting cells and from circulation. $\endgroup$
    – Riq
    Feb 16, 2022 at 18:54

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