How to manage HSV risk

I

ingrid

New member
I'm (she/her) in a long-term poly relationship with my partner Y (he/him). Y has a newish partner, X (she/her). Things have been going well and it looks like X could become a long-term partner for him.

I'm looking for advice/experiences/viewpoints on how to manage the approach to avoid HSV risk and (lack of) barriers. I know a lot comes down to personal risk tolerance and there are no right or wrong answers!

X has tested positive for both HSV-1 and HSV-2 (antibody testing). Her HSV-2 symptoms were mild enough to go initially unconfirmed. Her public healthcare provider wouldn't test her. She hasn't had symptoms ever since.

Y is negative for both (antibody testing).

My status is unknown. I've never been tested for either. I have never had any a known exposure, or any symptoms. My concerns are mainly focused on HSV-2, as I'm probably more likely to be asymptomatic carrier of HSV-1 than not. (Kissing people is fun.)

Somewhat complicating the situation is that I've got extremely low IgA-mediated immunity. According to my GP, this is a chronic condition that can result in various autoimmunity issues, as well as a poorer function of immunity, particularly in the mucous membranes (e.g. mouth & respiratory track, gut, and, you guessed it - genitals), which may affect my ability to resist and clear infections. This is a selective deficiency (my IgG level is normal, for example), so I don't consider myself immunocompromised. However, this makes me consider the HSV-2 risk as a potentially a bit more serious issue. That X had an easy time with it doesn't guarantee that I would.

Y and I are currently not using any barriers (fluid-bonded, if you wish) and we both really enjoy it. Y would obviously be happy if I felt like reintroducing barriers temporarily or more permanently, but I'd feel sad to do so for the foreseeable future.

X & Y have been using barriers for penetrative sex and oral sex (dental dams and condoms) but they do engage in kissing. Y feels that the barriers for oral are, therefore, pointless.

None of us currently have other partners that we would be sexual with, but we're not closed, so that may be something to consider, as well, as it's likely to happen sooner or later.

I'm currently leaning towards continuing to have unbarriered sex with Y unless he tests positive, in which case we can reassess. I'm aware that he may get a false positive, or have infected me before his next round of testing (every 3 months). I'm also aware that condoms and other barriers aren't a 100% protection against HSV.

I'm not sure how I feel about Y wanting to remove barriers for oral sex with X, particularly the dental dams, as my understanding is that he could still catch HSV-2 (vulva to mouth) and give it to me through unprotected (mouth to vulva) oral which could potentially cause recurrent outbreaks in me, if I'm unlucky and don't fight the virus as well as X. (My understanding is that HSV-1 is less likely to cause bothersome recurrent outbreaks in the genitalia, although it's not impossible. Correct me if I'm wrong.)

But maybe I should just suck it up, let them remove whichever barriers they want to remove, and accept that there will always be a risk of STIs if one is sexually active, and even if I got a more aggressive/recurrent case, it might suck, but I'm not going to die? Neither X or Y have any shown any sort of reckless behaviour (quite the contrary) so I don't believe they would have sex while prodromal/symptomatic because they don't care about my health, for instance. That would be out of character.

I would be very grateful for thoughts and viewpoints, as this is a somewhat new situation to me. Although none of us are new to poly, I've never had to look into HSV-2 risk management before and am cognizant that I may be missing some essential information about the topic.
 
Hi Ingrid,

In many communities surveyed via blood donation HSV-1 & 2 status is positive for the greater proportion of the samples from those over 40yrs. Navigating HSV risk is something most of us are likely doing whether we know it or not. Knowing and being honest about status seems like a credit to your connections. Maybe, consider confirming your status if the cost is not prohibitive?

Your research has no doubt revealed that viral shedding by an asymptomatic carrier can potentially lead to infection. However, avoiding contact while symptomatic (including prior to visble lesions when localized pain may predict an outbreak) appears to have been successful in avoiding transmission in many long-term relationships, some for decades. HSV-1 has become more prevalent recently and healthcare providers aren't usually given to assuming HSV1 vs HSV2 based on where the lesions appear.

With regard additional concerns stemming from your IgA deficit. For most HSV positive folks the virus is not a health concern and at most an episodic nuisance. Probably the biggest health concern with HSV infection historically was infection of a newborn (with an underdeveloped immune response) during birth. Since the approval of acyclovir and related antivirals for treatment of herpes virus infections, even this worst-case situation can be treated successfully. Should an HSV infection manifest then access to these antivirals would manage symptoms in most individuals with reduced immunity. Someone experiencing regular outbreaks can reduce or abolish these (and dramatically reduce transmission risk) with preventative oral antivirals. Acyclovir is generally well tolerated and for many it's free of side effects.

I hope this is helpful.
 
I have HSV-1 and take Acyclovir as needed when I suspect a breakout. However I know some HSV-2 folks who take Acylovir daily to prevent outbreaks and protect their partners from infection. I would suggest that the partner talk to their doctor about options.

Dental dams can help with some types of STI's but condoms are not very effective with HSV.
 
Hello ingrid,

The only ways I know of, to manage HSV risk, are a) use barriers if you can, and b) get tested regularly. Well and there's abstinence, but I don't think that's possible in this situation.

Wikipedia may help.
Regards,
Kevin T.
 
Stem said:
Hi Ingrid,

In many communities surveyed via blood donation HSV-1 & 2 status is positive for the greater proportion of the samples from those over 40yrs. Navigating HSV risk is something most of us are likely doing whether we know it or not. Knowing and being honest about status seems like a credit to your connections. Maybe, consider confirming your status if the cost is not prohibitive?

Your research has no doubt revealed that viral shedding by an asymptomatic carrier can potentially lead to infection. However, avoiding contact while symptomatic (including prior to visble lesions when localized pain may predict an outbreak) appears to have been successful in avoiding transmission in many long-term relationships, some for decades. HSV-1 has become more prevalent recently and healthcare providers aren't usually given to assuming HSV1 vs HSV2 based on where the lesions appear.

With regard additional concerns stemming from your IgA deficit. For most HSV positive folks the virus is not a health concern and at most an episodic nusiance. Probably the biggest health concern with HSV infection historically was infection of a newborn (with a naive underdeveloped immune response) during birth. Since the approval of acyclovir and related antivirals for treatment of herpes virus infections even this worst case situation can be treated successfully. Should an HSV infection manifest then access to these antivirals would manage symptoms in most individuals with reduced immunity. Someone experiencing regular outbreaks can reduce or abolish these (and dramatically reduce transmission risk) with preventative oral antivirals. Acyclovir is generally well tolerated and for many it's free of side effects.

I hope this is helpful?
Click to expand...
Update: I did a quick check of the literature regarding IgA deficiency and HSV. IgA deficiency has not been associated with more severe disease or a higher frequency of outbreak recurrence in those infected. Whereas IgG deficiencies have been associated with these negative outcomes. My search wasn't exhaustive, but what I found seems reassuring in your case.
 
Stem said:
Update: I did a quick check of the literature regarding IgA deficiency and HSV. IgA deficiency has not been associated with more severe disease or a higher frequency of outbreak recurrence in those infected. Whereas IgG deficiencies have been associated with these negative outcomes. My search wasn't exhaustive, but what I found seems reassuring in your case.
Click to expand...
Sorry I somehow didn't get a notification for this! Thanks so much for looking it up, that's indeed reassuring. :)

If you do have a way of easily finding that reference I'd be curious to read it - I somehow didn't find it myself!
 
Update:
I've decided that the small additional risk from unprotected oral is acceptable to me, particularly as it seems important for X and she has felt stigmatized against (which I really don't want!). It's impossible to meaningfully eliminate the risk entirely in our setting, so getting too hung up on some minor % doesn't feel fruitful. We can always re-evaluate barrier use (between Y and me, and/or X and Y) if X has further outbreaks or Y tests positive. Same for antivirals - we investigated that route but given that X hasn't had further outbreaks it doesn't seem necessary, but they remain an option should something change

I'm really thankful for all of your knowledgeable answers; it's been great to have a safe and neutral space to discuss this.
 
Hi ingrid,

Thanks for that update, it sounds like you have a solid plan for risk management. Let us know if we can be of further help.

Regards,
Kevin T.
 
ingrid said:
Sorry I somehow didn't get a notification for this! Thanks so much for looking it up, that's indeed reassuring. :)

If you do have a way of easily finding that reference I'd be curious to read it - I somehow didn't find it myself!
Click to expand...
Hi, sorry for the delay!

I've pasted some of the research paper details below with abstracts. I don't know how many of these are open-access. I'll keep an eye out for others:

Subtly Impaired Humoral Immunity Predisposes
to Frequently Recurring Genital Herpes Simplex
Virus Type 2 Infection and Herpetic Neuralgia
Mikko Seppa¨nen,1 Seppo Meri,4 Irma-Leena Notkola,7 Ilkka J. T. Seppa¨ la¨ ,4 Eija Hiltunen-Back,2 Heikki Sarvas,4
Maija Lappalainen,5 Hannamari Va¨ limaa,5 Anil Palikhe,6 Ville V. Valtonen,1 and Marja-Liisa Lokki6
1Division of Infectious Diseases, Department of Medicine, 2Department of Dermato-Venereology, and 3Department of Virology, Laboratory Division,
Helsinki University Central Hospital, Hospital District of Helsinki and Uusimaa, Departments of 4Bacteriology and Immunology and 5Virology
and 6HLA Laboratory, Transplantation Laboratory, Haartman Institute, University of Helsinki, and 7Department of Epidemiology and Health
Promotion, National Public Health Institute, and National Research and Development Centre for Welfare and Health, Helsinki, Finland
Background. Immunogenetic factors predisposing to recurrent genital herpes remain poorly characterized.
Methods. In a prospective case-control study, 52 consecutive patients with frequently recurring outbreaks of
genital herpes were compared with 80 herpes simplex virus (HSV)–seropositive (types 1 and 2) and 70 HSVseronegative
control subjects. Immunoglobulins (Igs), type-specific anti–HSV-2 IgG and IgG subclass antibodies
against glycoprotein G, levels of C3 and C4, and classical pathway hemolytic complement activity were measured,
and IgG1 and IgG3 allotyping; C4 immunophenotyping; C4* real-time polymerase chain reaction (PCR) genotyping;
and HLA-A*, B*, and DR* typing were performed.
Results. The G3mg,G1ma/a(x) haplotype was more frequent in patients than in HSV-seronegative control subjects
(Pp.047). Compared with all control subjects, low levels of total IgG1 (odds ratio [OR], 4.9 [95% confidence
interval {CI}, 2.0–12.5]; Pp.001) and IgG3 (OR 3.6 [95%CI 1.7–7.8]; Pp.001), but not of anti–HSV-2 antibodies,
were associated with recurrences. Levels of complement were lowest in patients. The C4* null type was negatively
associated with neuralgia (OR, 0.2 [95% CI, 0.06–0.81]; Pp.022).
Conclusions. Low levels of antibody-dependent cellular cytotoxicity–mediating IgG1 and IgG3 antibodies,
partly dependent of allotype, may predispose to recurrent genital herpes. Antibodies produced by T helper type
1 responses, potentially against an unknown epitope, appear to be relevant in recurrences. In patients, C4*
deficiencies are associated with protection from herpetic neuralgias, possibly through reduced inflammation.

Host Genetic Factors in Susceptibility to Herpes Simplex
Type 1 Virus Infection: Contribution of Polymorphic Genes at
the Interface of Innate and Adaptive Immunity
Manuela Moraru,* Elisa Cisneros,* Natalia Go´mez-Lozano,* Rosario de Pablo,*
Francisca Portero,† Marı´a Can˜izares,* Mercedes Vaquero,‡ Gasto´n Rousta´n,x Isabel Milla´n,{
Miguel Lo´pez-Botet,‖ and Carlos Vilches*
HSV-1 establishes life-long latency that can result in clinical relapses or in asymptomatic virus shedding. Although virtually all
adults have been exposed to HSV-1, the clinical course varies remarkably. Genetic host variability could be related to this clinical
diversity. In this study, we analyzed the contribution of gene families in chromosomes 1, 6, 12, and 19, which encode key regulators of
the innate and adaptive immunity, in a cohort of 302 individuals. Class I and class II alleles of the HLA system, the copy-number
variation of NK cell receptor genes (KIR and NKG2C), the combinations of killer cell Ig-like receptor and their HLA ligands, and
CD16A and CD32A allotypes of variable affinity for IgG subclasses were all studied. Although no major susceptibility locus for
HSV-1 was identified, our results show that the risk of suffering clinical HSV-1 infection is modified by MHC class I allotypes
(B*18, C*15, and the group of alleles encoding A19), the high-affinity receptor/ligand pair KIR2DL2/HLA-C1, and the CD16A-
158V/F dimorphism. Conversely, HLA class II and CD32A polymorphisms and NKG2C deletion did not seem to influence the
clinical course of herpetic infection. Collectively, these findings support an important role in host defense against herpetic infection
for several polymorphic genes implicated in adaptive immunity and in surveillance of its subversion. They confirm the crucial role
of cytotoxic cells (CTL and NK) and the contribution of genetic diversity to the clinical course of HSV-1 infection. The Journal of
Immunology, 2012, 188: 4412–4420.

Immunity to vaginal HSV-2 infection in immunoglobulin A knockout mice
M. B. PARR,* G. R. HARRIMAN† & E. L. PARR* *Southern Illinois University, School of Medicine, Carbondale, IL and
†Mount Sinai Medical Center, Miami Beach, FL, USA
SUMMARY
An immunoglobulin A (IgA) knockout (KO) mouse was used to study the role of IgA in
protective immunity against vaginal infection with herpes simplex virus-type 2 (HSV-2). Intact
and KO mice were immunized intravaginally (IVAG) with attenuated HSV-2, challenged IVAG
with wild-type virus 6 weeks later and evaluated for vaginal infection and neurological disease.
Non-immunized/challenged intact and KO mice showed vaginal infection and succumbed to
neurological disease, while immunized/challenged mice exhibited reduced or no vaginal infection
and no neurological disease. Log 2·5 enzyme-linked immunoassay (ELISA) titres of viral IgA,
immunoglobulin G (IgG) and immunoglobulin M (IgM) in vaginal secretions collected from
intact immune mice before challenge were 0·6±0·3, 6·4±0·32 and 0·0, while those in KO immune
mice were 0·0, 6·7±0·19 and 3·0±0·29, respectively. Twenty-four hours after challenge, the
percentage of vaginal epithelium that was infected in non-immune intact and KO mice was
2·0±0·6 and 2·4±0·6, which was reduced to 0·2±0·1 and 0·1±0·06 in immune intact and KO
mice, respectively. No shed virus protein was detected in vaginal secretions 3 days after challenge
in any immune mouse, whereas titres were 1400 and 1700 in the two groups of non-immune mice.
Thus, immune protection against vaginal HSV-2 infection was similar in both KO and intact
mice, indicating that this mucosal immunity does not depend mainly on IgA.

HLA-DRB1*01 allele and low plasma immunoglobulin G1 concentration may
predispose to herpes-associated recurrent lymphocytic meningitis
Katariina Kallio-Laine a,b,*, Mikko SeppÅnen c, Janne Aittoniemi d, Hannu Kautiainen b,e, Ilkka SeppÅlÅ f,
Ville Valtonen c, Markus FÅrkkilÅ g, Eija Kalso a, Marja-Liisa Lokki h
a Pain Clinic, Department of Anaesthesiology and Intensive Care Medicine, Helsinki University Central Hospital, Helsinki, Finland
b Orton Orthopaedic Hospital, Orton Foundation, Helsinki, Finland
c Immunodeficiency Unit, Division of Infectious Diseases, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland
d Department of Clinical Microbiology, Centre for Laboratory Medicine, Pirkanmaa Hospital District, Tampere, Finland
e Family Practice Unit, Central Finland Central Hospital, Jyvãskylã, Finland
f Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki and Laboratory Division, Helsinki University Central Hospital, Helsinki, Finland
g Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland
h Transplantation Laboratory, Haartman Institute, University of Helsinki, Helsinki, Finland
A R T I C L E I N F O
Article history:
Received 22 May 2009
Accepted 22 October 2009
Available online 30 October 2009
Keywords:
Lymphocytic meningitis
Herpes simplex virus type 2
IgG deficiency
Complement C4
HLA genes
A B S T R A C T
Recurrent lymphocytic meningitis (RLM) is a rare illness caused mostly by herpes simplex virus type 2
(HSV-2). Predisposing factors are not known. Deficiencies in immunoglobulin (Ig) G subclasses 1 (IgG1)
and 3 (IgG3) and complement protein C4 are associated with susceptibility to and persistence of bacterial
and viral infections. Selected HLA and mannose-binding lectin (MBL) alleles have previously been
associated with recurrent genital herpes or herpetic meningitis. We assessed the frequencies of low IgG1
and IgG3, their allotypes (Gm), and HLA-A*, -B*, -DRB1*, and MBL2 alleles, as well as deficiencies in C4A
and C4B genes, as potential predisposing factors for HSV-2-associated RLM. The level of IgG1 was lower
(p 0.009) and the frequency of low IgG1 was higher (p 0.001) in patients than in controls.
Furthermore, the risk for a new meningitis episode was increased in patients with low IgG1 (incident
ratio 2.05). HLA-DRB1*01 (p 0.009) and -B*27 (p 0.050) were more common among patients than
controls. We conclude that HLA-DRB1*01 and -B*27 alleles and low plasma IgG1 levels may be significant
risk factors for RLM.
 
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