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We investigated the role of antibodies against the mature portion of glycoprotein G (mgG-2) of herpes simplex virus 2 (HSV-2) in protective immunity after vaccination.
This editable Main Article is under development and not meant to be cited; by editing it you can help to improve it towards a future approved, citable version. Herpes, also called herpes simplex, is any of the diseases caused by herpes simplex virus (HSV). There are two subtypes of the virus that can each be responsible for either cold sores or genital herpes; although human herpesvirus 1 (herpes simplex virus-type 1 or HSV-1) is the overwhelmingly common cause of cold sores, and HSV-2 is responsible for a slight majority of genital herpes cases. Herpes simplex virus (HSV) is a member of the Herpesviridae family of viruses, a family of DNA viruses. UI: 14624112) HSV 1 and 2 correspond to HHV 1 and 2, and both are very prevalent in the human population, with as many as 30-70% of all people tested testing positive for antibodies at some point in their lifetime. HSV's genome is a double stranded linear DNA, with about 50% sequence homology between HSV-1 and HSV-2. Active replication of the virus in these cells results in the lesions of typical vesicles and shedding of the virus. The virus is destroyed, except for virus which, through retrograde axonal transport, is sequestered in the ganglion of sensory neurons. All symptoms of infection disappear at that point and the infected person enters a period of "latent infection". Even during latent infections, when there are no symptoms or signs of illness, the virus is maintained in a repressed state in nerve cells. Herpes Simplex viruses generally cause mucocutaneous infection, that is, cells of the skin and the mucous membranes are infected. The initial infection with the virus is called the primary infection, and can be accompanied by systemic systems such as fever and muscle aches. In general, lesions from HSV 1 are more commonly seen on the face, but also accounts for a large minority of genital infections. Transmission can occur when sores are visible, as well as when there are no visible lesions. The diagnosis of a herpes simplex infection is ordinarily a clinical one, that is- it is made by a trained health care provider based on the patient's history and physical findings, rather than on laboratory tests.
Viral culture is an expensive laboratory test that must be carried out for 10 days in order to assume negative results. These cell culture dishes are pictured from a laboratory performing culture of herpes simplex virus.
Diagnostic tests on the immune response to the virus can determine not only the subtype of herpes simplex infection but whether the outbreak is primary or recurrent. HSV-1 and HSV-2 each have respective variations in virally produced glycoprotein G, and immunoglobulin G (IgG) produced by an infected person differs accordingly. Cold sores are most commonly caused by Human herpesvirus 1 and are ubiquitous in distribution in human populations. In population studies in the United States, both serotypes of the herpes virus are prevalent in symptomatic genital herpes infections. Although both types of herpes simplex virus can account for genital herpes, and cause a very similar appearing rash, "HSV-1 has a much lower recurrence rate.
The Center for Disease Control (CDC) in the United States recommends that genital lesions be cultured in order to determine the type of HSV infection, since the severity and clinical course of the disease can be better predicted with this information. There is a relationship between genital herpes and the risk of catching (and spreading) additional venereal diseases, since the ulcers caused by herpes are more vulnerable to invasion by pathogens than intact skin or mucosa.
Although herpes infection is aggravating in healthy adults, it is a lethal disease in very young babies.
However, newborns have a limited immune system for the first 3 weeks of life, and even a kiss by a well-meaning friend or relative who bears a virus-shedding cold sore on the lips can cause infection in the newborn (albeit rarely).
All the immunosuppressive drugs used to allow transplant patients to keep their transplanted organs healthy have an unfortunate side effect of reactivating latent herpes simplex infections. Herpes has been recognized for centuries, "cold sores" (herpes febrilis) were described by the Roman physician Herodotus in the year 100 CE. Mice were immunized intramuscularly with mgG-2 and oligodeoxynucleotides containing two CpG motifs plus alum as adjuvant.
IntroductionHerpes simplex virus 2 (HSV-2) infects the genital mucosa and establishes a life-long infection in dorsal root sensory ganglia (DRG).
StatisticsSigmaPlot 12 software [20] for Microsoft Windows was used for statistical calculations. Discussion We show that anti-mgG-2 antibodies, elicited after vaccination of mice with mgG-2 and adjuvant, are important for the outcome after genital challenge with HSV-2.
The phenomenon of latent infection permits long-term persistence of the virus within the host and potential future transmissibility to others."[1] Other species of Herpes virus are also human pathogens, notably Herpes Zoster, the cause of both chicken pox (in acute infection) and shingles (chronic infection with reactivation).
Many of the polypeptides produced by each type of virus are identical, and are coded by the homologous regions of DNA, but some of the expressed proteins are different and some of these distinct proteins are antigenic - that is, they give rise to an antibody response in infected hosts. During this time, special tests done in research can demonstrate single strand viral RNA in the infected nerves. In addition to the common mucocutaneous infection, HSV 1 and 2 can also cause keratitis (inflammation in the eye), encephalitis (brain infection), and severe neonatal disease if acquired during pregnancy.
However, a clinical diagnosis does not distinguish between HSV-1 and HSV-2 infection, except by probability.

Because HSV 2 is spread more commonly by sexual contact, it is easier to prevent than HSV 1. After primary infection HSV-2 reactivates and may cause recurrent and painful genital ulcerations, or more commonly asymptomatic shedding. Proliferation of cells and production of IFN-? in the supernatant from the cell culture proliferation assay were measured. When mice were immunized im ? three with CpG and alum as adjuvant, complete protection from death and disease was observed.
Serological testing for such antibodies is the usual means to determine the type of HSV (1 or 2) infection present in patients. Although genital lesions are a form of STD, other lesions can be contracted without sexual contact. Confirming a diagnosis and clarifying the actual virus type involve requires laboratory testing.
If the individual has clear signs of a genital herpes infection, but the tests for IGG are negative, the most likely explanation is that this is a primary outbreak, and the patient has not yet begun production of that type of antibody. More than 50 million people are infected in that country, making this the most common STD in the USA. High levels of immunoglobulin G subclass 1 (IgG1) and IgG2 antibodies were detected and re-stimulated splenic CD4+ T cells proliferated and produced IFN-?.
According to estimations of World Health Organization more than 500 million individuals are infected globally [1]. Thus, we show that anti-mgG-2 antibodies contribute to protection after vaccination with mgG-2.
First, sera were collected from im immunized mice using CpG and alum as adjuvant and, second, mice immunized with sc plus in administrations using CpG as adjuvant.
These adjuvants in combination with different subunit HSV-2 antigens given im have been used successfully to elicit robust B- and T-cell immune responses [21,22].
Regardless of how they were contracted, however, an infected person can spread virus to another person with mucosa to mucosa or skin to mucosa contact. The most definitive proof of infection, the "gold standard" of diagnostic tests, is the growth of the virus in artificial culture from a specimen taken from the patient's lesions. Confirmation of that presumed diagnosis of a primary herpes infection can be made on follow-up testing, with demonstration of anti-HSV IgG levels. None of the sera from immunized mice exhibited neutralization, while all sera exerted antibody-dependent cellular cytotoxicity (ADCC) and complement-mediated cytolysis (ACMC) activity. Moreover, HSV-2 infection is associated with a significant increased risk of HIV acquisition. Proliferation was measured by radiolabeled thymidine incorporation and presented as SI units. Although primary ulcers have a high rate of viral shed, recurrent lesions shed virus at a much lower rate, and so culture of recurrent lesions has a high false negative rate. We conclude that anti-mgG-2 antibodies after vaccination significantly increased the production of IFN-? and reduced the viral load in vaginal washes. Despite high IgG1 titers, none of the sera showed NT activity with or without complement (titer < 20) (Table 1). Thus, our data emphasize the importance of the adjuvant and the administration protocol used together with the mgG-2 antigen. UI: 9674772), and reactivation of the virus from sacral nerves is the basis for recurrent genital herpes. Accordingly, in patients with typical presentations of recurrent outbreaks, failure to culture the virus in no way overturns the diagnosis. Despite promising data from animal studies, results in vaccine clinical trials have been discouraging with limited or no protection against HSV-2 infection or disease [2,3,4,5]. For 10 mice, using the im immunization protocol, sufficient volumes were available for the ADCC assay. Sera from mice that were vaccinated subcutaneously and intranasally with mgG-2 presented significantly lower titers of IgG antibodies and lower ADCC and ACMC activity.
An estimate of the global prevalence and incidence of herpes simplex virus type 2 infection. We conclude that anti-mgG-2 antibodies were of importance to limit genital HSV?2 infection. Mice vaccinated with CpG and alum and mgG-2 and alum, all showed severe disease and succumbed after challenge before day 14 post infection.
NT, ADCC and ACMC Activity of Anti-mgG-2 AntibodiesIn the present study, as described in our earlier report [11], no NT activity in the presence or absence of complement was detected in immune sera.
ADCC and ACMC activity are potentially important mechanisms in protective immunity, and could tentatively be evaluated in future animal vaccine studies and in clinical trials. The latter portion is matured by heavy O-glycosylation in mammalian cells and contains several clusters of single N-acetyl galactosamine with affinity for Helix pomatia (HPA) lectin. Different anti-mgG-2 MAbs and rabbit immune serum raised against purified mgG-2 also lack NT activity [11,12,23,24]. Both gG-2 proteins elicit exclusively type-specific antibody responses in humans [6,7,8,9,10], and mgG-2 is commonly used as antigen for serodiagnosis of HSV-2 infection in clinical settings. The results presented herein suggest that anti-mgG-2 antibodies are involved in protective immunity by other functional properties than NT activity.

We showed earlier that subcutaneous (sc) and intranasal (in) immunization with a prophylactic vaccine based on mgG-2 and CpG induced partial protection (73% survival) in a mouse genital model [11], and that protection was associated with the IFN-? production by CD4+ T cells. Few studies on ADCC have been performed in mice, probably due to difficulties in preparation of effector cells and weak responses. A novel finding was that a majority of immune sera exerted antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent complement-mediated cytolysis (ACMC) activity, but no neutralization (NT) activity. Although no obvious correlations between NT activity and protection are described in animal studies [12,13], and vaccine clinical trials [4,5], NT activity has often been used as a marker of the antibody responses. In a recent follow-up report from GSKs clinical trial of HSV negative women (Herpevac Trial), vaccinated with gD-2, 82% protection was observed against HSV-1 genital disease.
Interestingly, the antibody levels against gD-2, but not the cellular immune responses, correlated to immune protection [14]. Furthermore, neutralizing antibody titers were significantly higher to HSV-1 than to HSV-2, an observation that may explain the failure to protect against HSV-2 infection [15]. These data justify studying the role of antibodies in protection in other vaccine candidates. In this study, all sera from im immunized mice showed ADCC and ACMC activity, while approximately half of the sera collected from mice with immunization protocol using sc plus in administrations.
We here evaluated the role of anti-mgG-2 antibodies in the clearance of genital HSV-2 infection, and for induction of protective immunity after vaccination. However, we cannot exclude that the addition of alum as adjuvant in combination with im immunization route induce a different antibody profile that is more disposed to induce ADCC and ACMC activity. We also evaluated whether the immunization protocol modified IgG titers and ADCC and ACMC activity by comparing intramuscular with sc plus in administrations. Further studies using Fc?-receptor and complement depleted mice are warranted to investigate the biological relevance of ADCC and ACMC for protection against genital infection and disease in mgG-2 immunized animals.
Ethics StatementThis study was carried out in accordance to the rules stated by the Swedish board of agriculture.
Cells and VirusesAfrican green monkey kidney (GMK-AH1) cells were cultured in Eagle's minimal essential medium supplemented with 2% calf serum and antibiotics. Baby hamster kidney (BHK21) cells were propagated in Glasgow minimum essential medium with 8% calf serum, 1% L-glutamine, and 8% tryptose phosphate broth. Passive Transfer of Antibodies to Naive MiceSeveral studies have described that passive transfer of polyclonal immune serum to non-immunized mice or guinea-pigs does not prevent HSV-2 infection but reduces genital and neurological disease, and in the guinea-pig model also subsequent recurrent shedding [25,30,32,33].
Similar results have been described using passive transfer of MAbs directed against gB or gD followed by i.vag. However, passive transfer of anti-HSV-2 serum to naive mice was not so effective in preventing death and local replication in an ocular challenge model with HSV-2 [36].
The discordant results may be explained by differences in the amount and specificity of antibodies given, virus dose, and the challenge model used.
The concentration of mgG-2 specific IgG antibodies was analyzed in an ELISA using a standard curve created by a mixture of the MAbs. Results presented in this study suggest that anti-mgG-2 antibodies are protective in immunized mice most likely together with T cells but ineffective acting alone. Concluding RemarksData presented in this report suggest that mgG-2 has an important, but to date unknown function, in the genital infection, which can be targeted by immune responses elicited after vaccination.
The results emphasize the importance of inducing antibodies after vaccination, and may result in a paradigm shift in the understanding of the correlate of protection [38].
Non-neutralizing antibodies which contribute to protection, possibly mediated by ADCC or other humoral effector functions, have been described not only for HIV, but also for other RNA and DNA viruses [39]. The generation of antibodies, which present ADCC and ACMC activity, may therefore be relevant in the development of vaccines against HSV-2 infection.
IgG antibodies against mgG-2 were detected by an indirect ELISA as previously described [9,11]. Anti-mouse subclass-specific peroxidase-conjugated IgG were used as conjugates (Southern Biotech, Birmingham, AL, USA) at a 1:1000 dilution. The antibody titer was defined as the reciprocal value of the highest serum dilution giving an optical density (OD) greater than a negative serum plus 0.2 OD units. CD4+ T Cell Proliferation Assay and Cytokine DetectionThe assay is described in detail elsewhere [11]. CD4+ T cells were purified using the BD IMag™ Mouse CD4+ T Lymphocyte Enrichment Set (BD Bioscience, Stockholm, Sweden). Cells were labeled with 1 µCi of [6-3H3]thymidine (Amersham Biosciences, Piscataway, NJ, USA), and incubated overnight.
Cell proliferation was expressed as mean stimulation index (SI), defined as the amount of [6-3H3]thymidine incorporated into antigen-stimulated cultures divided by the mean amount incorporated into corresponding unstimulated control cultures.
Antibody Dependent Cellular Cytotoxicity (ADCC) and Complement-Mediated Cytolysis (ACMC)ACMC was performed as described while for the ADCC assay we used a slightly modified method from what have previously been described [11].
After preparation macrophages were re-suspended in Iscoves with 5% inactivated foetal calf-serum, and 1% antibiotics. Effector cells were added, followed by incubation for 18 h at 37 °C in a humid atmosphere of 5% CO2.

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