Sexual Transmission and the Natural History of Human Herpesvirus 8 Infection
Jeffrey N. Martin, M.D., M.P.H., Donald E. Ganem, M.D., Dennis H. Osmond, Ph.D., Kimberly A. Page-Shafer, Ph.D., Don Macrae, B.S., and Dean H. Kedes, M.D., Ph.D.
Background Although human herpesvirus 8 (HHV-8) has been suspectedto be the etiologic agent of Kaposi's sarcoma, little is knownabout its seroprevalence in the population, its modes of transmission,and its natural history.
Methods The San Francisco Men's Health Study, begun in 1984,is a study of a population-based sample of men in an area witha high incidence of human immunodeficiency virus (HIV) infection.We studied all 400 men infected at base line with HIV and asample of 400 uninfected men. Base-line serum samples were assayedfor antibodies to HHV-8 latency–associated nuclear antigen(anti-LANA). In addition to the seroprevalence and risk factorsfor anti-LANA seropositivity, we analyzed the time to the developmentof Kaposi's sarcoma.
Results Anti-LANA antibodies were found in 223 of 593 men (37.6percent) who reported any homosexual activity in the previousfive years and in none of 195 exclusively heterosexual men.Anti-LANA seropositivity correlated with a history of sexuallytransmitted diseases and had a linear association with the numberof male sexual-intercourse partners. Among the men who wereinfected with both HIV and HHV-8 at base line, the 10-year probabilityof Kaposi's sarcoma was 49.6 percent. Base-line anti-LANA seropositivitypreceded and was independently associated with subsequent Kaposi'ssarcoma, even after adjustment for CD4 cell counts and the numberof homosexual partners.
Conclusions The prevalence of HHV-8 infection is high amonghomosexual men, correlates with the number of homosexual partners,and is temporally and independently associated with Kaposi'ssarcoma. These observations are further evidence that HHV-8has an etiologic role in Kaposi's sarcoma and is sexually transmittedamong men.
Among persons infected with the human immunodeficiency virus(HIV), the disproportionate incidence of Kaposi's sarcoma amonghomosexual or bisexual men has long suggested that a sexuallytransmitted cofactor, in addition to background HIV infection,is responsible for the development of Kaposi's sarcoma.1 A novelherpesvirus, termed human herpesvirus 8 (HHV-8) or Kaposi'ssarcoma–associated herpesvirus, became a candidate forthe etiologic cofactor when its DNA sequences were discoveredin tissue specimens of Kaposi's sarcoma.2 Subsequently, thedetection of HHV-8 DNA sequences in all forms of Kaposi's sarcoma3,4,5,6,7has strengthened the biologic argument. Cross-sectional epidemiologicstudies have determined that HHV-8 seropositivity in variouspopulations is strongly correlated with the population's riskof Kaposi's sarcoma,8,9,10,11,12 and a few longitudinal studieshave shown that HHV-8 infection precedes the onset of Kaposi'ssarcoma.13,14,15 Longitudinal studies are critical in the evaluationof causality, because they exclude the possibility that HHV-8infection is the result rather than the cause of Kaposi's sarcoma.Definitive epidemiologic evidence, however, requires longitudinalobservation for Kaposi's sarcoma with careful control for potentialconfounding factors such as the patient's degree of sexual exposure,degree of immunocompromise, and geographic area of residenceand changing temporal trends in HHV-8 seroprevalence.
If HHV-8 is assumed to be the cause of Kaposi's sarcoma, itbecomes imperative to understand its distribution within populations,its modes of transmission, and its natural history. The highprevalence of infection among homosexual or bisexual men inthe United States has suggested that HHV-8 may be sexually transmitted.8,9,11The available studies, however, offer only indirect evidenceof sexual transmission, because they have not correlated individualsexual behavior with HHV-8 infection.
To address several unresolved aspects of HHV-8 infection, weused data from the San Francisco Men's Health Study. This studyenrolled a population-based sample of men residing in an areaof high HIV incidence for whom detailed behavioral historiesand 10-year follow-up for the development of Kaposi's sarcomaare available. We present population-based estimates of theseroprevalence of HHV-8 and further data that support an independentassociation of HHV-8 infection with Kaposi's sarcoma.
Methods
Population and Sampling
The San Francisco Men's Health Study was initiated to studythe natural history of HIV infection.16 The target populationwas unmarried men in San Francisco at high risk for HIV infection.Study sampling has been described in detail elsewhere.17 Inbrief, there was stratified two-stage cluster sampling of allhouseholds in the 19 census tracts in San Francisco with thehighest incidence of the acquired immunodeficiency syndrome(AIDS) through 1983. First, a sample of blocks was chosen fromeach tract with probability proportionate to the estimated numberof households on each block. Second, a sample of householdswas randomly selected from each block. In each household, allunmarried men 25 to 54 years of age were invited to enroll.At base line, from June 1984 through January 1985, 1034 menwere interviewed and had biologic specimens collected. Eighthundred twenty-two men reported themselves to be homosexualor bisexual, and 212 reported that they were exclusively heterosexual.At base line, 400 men were HIV-seropositive, 624 were HIV-seronegative,and 10 refused testing. No exclusively heterosexual man wasHIV-seropositive. Subsequently, the men were followed at six-monthintervals through 1994, by which time AIDS had developed in63 percent of the men who were infected with HIV at base line.The current study of HHV-8 infection included all 400 men whowere infected with HIV at base line, a random sample of 200of the 422 homosexual or bisexual men who were not infectedwith HIV at base line, and 200 of the 212 exclusively heterosexualmen.
Epidemiologic, Behavioral, and Immunologic Variables
The base-line questionnaires requested information on demographics,self-reported medical history (including sexually transmitteddiseases and transfusions), and illicit-drug use. On the basisof their self-reported sexual practices during the previousfive years, the men were classified as exclusively homosexualor exclusively heterosexual or were placed into one of threeintermediate bisexual categories (Table 1). They were also askedhow many male and female sexual-intercourse partners they hadhad during the previous two years, and when they started tohave intercourse regularly. Intercourse was defined as any insertiveor receptive act in which a man's penis was placed into anotherperson's mouth, vagina, or anus. Analysis of lymphocyte subpopulationswas performed with standard techniques.18
Table 1. Population-Based Estimates of the Prevalence of HHV-8 Anti-LANA Antibodies According to Sociodemographic Characteristics, Sexual Orientation, and HIV Serologic Status.
Antibodies to HHV-8
Base-line serum samples that had been stored at -70°C weretested in a blinded fashion for evidence of HHV-8 infectionby a previously described indirect immunofluorescence assaythat measures antibodies to a latency-associated nuclear antigen(anti-LANA).8 This assay uses as its substrate isolated nucleifrom a cell line, BCBL-1, that is latently infected with HHV-8and not infected with the Epstein–Barr virus. After incubationwith 1:40 diluted test serum, unbound antibody is washed away,and a secondary antibody, Texas red–conjugated goat antihumanIgG, is added. Samples are considered anti-LANA–positiveif they produce a punctate nuclear pattern in all BCBL-1 nucleivisualized but not in parallel testing with an HHV-8–uninfectedRamos cell line. All samples that tested anti-LANA–positivewere blindly retested, along with a random sample of those thatinitially tested anti-LANA–negative. Samples that produceddisparate results (less than 1 percent of the subjects) weretested a third time, and the majority outcome was taken as final.
Diagnosis of Kaposi's Sarcoma
At each follow-up visit, the subjects were asked whether Kaposi'ssarcoma had been diagnosed by their personal physicians in thepreceding interval. A physician's diagnosis, based on prevailingclinical practices, was considered to be evidence of Kaposi'ssarcoma in this study. The subjects also underwent a detaileddermatologic examination; those with suggestive lesions thathad not already been diagnosed as Kaposi's sarcoma were referredto their personal physicians or to dermatologists. Finally,all subjects were cross-referenced to a data base maintainedby the San Francisco Department of Public Health that activelypursued both AIDS-defining diagnoses and secondary AIDS-definingdiagnoses in all cases of AIDS in San Francisco.
Statistical Analysis
In addition to estimates of HHV-8 seroprevalence in the studysample, population-based seroprevalence was estimated by assigningprobability weights to each subject that took into account thesubject's original probability of selection according to censustract, the original response rate per census tract, and hisprobability of being selected for analysis in this substudyof HHV-8 infection. Variances were estimated by taking intoaccount these probability weights and the original block-clustersampling scheme.19,20
To determine the risk factors for HHV-8 infection, univariateanalyses of the associations between categorical variables andHHV-8 seropositivity were first evaluated with a chi-squaretest of independence. Multivariable logistic regression wasused to determine independent associations. Goodness of fitwas assessed by the Hosmer–Lemeshow test.21
Kaplan–Meier techniques were used to estimate the distributionof times from entry into the cohort to the diagnosis of Kaposi'ssarcoma according to base-line anti-LANA serologic status.22The distributions were compared by the log-rank test. Afteradjustment for potential confounders, the independent associationbetween HHV-8 and Kaposi's sarcoma was determined with multivariableproportional-hazards regression.23,24 All analyses were performedwith STATA (version 5.0)25 and SAS (version 6.11)26 software.
Results
Stored base-line serum was available for 397 of the 400 HIV-infectedsubjects in the San Francisco Men's Health Study. Of the 200subjects in the random sample of exclusively heterosexual men,none of whom were HIV-infected at base line, base-line serumwas available for 195. Of 200 homosexual or bisexual men whowere not HIV-infected at base line, base-line serum was availablefor 198. One subject had an indeterminate result on the anti-LANAassay on three separate readings and hence was eliminated fromsubsequent analyses; this resulted in 789 subjects availablefor analysis.
Population-Based HHV-8 Seroprevalence
The target population of the San Francisco Men's Health Studywas men at high risk for HIV infection early in the AIDS epidemicin San Francisco. Of the 789 men sampled, 223 (28.3 percent)had antibodies to HHV-8 LANA. To the extent that the cohortwas representative of the target population, the prevalenceof HHV-8 anti-LANA seropositivity can be extrapolated from thestudy sample to the target population (Table 1). In this population,the overall estimate of HHV-8 anti-LANA seroprevalence was 25.8percent (95 percent confidence interval, 22.6 to 29.1). HHV-8infection was not associated with age, race or ethnic group,or education but was associated in a graded fashion with thesubjects' self-reported degree of homosexual activity in theprevious five years. None of the 195 exclusively heterosexualmen were anti-LANA–seropositive, as compared, for example,with 12.5 percent of the men who reported some heterosexualbut mostly homosexual activity, and 39.6 percent of the menwho were exclusively homosexual (P<0.001 by chi-square testfor trend). HHV-8 seropositivity was also strongly correlatedwith base-line HIV infection (P<0.001). Among the homosexualor bisexual men, 189 of 396 HIV-infected men (47.7 percent)were anti-LANA–seropositive, as compared with 34 of 197HIV-uninfected men (17.3 percent) (P<0.001). The seroprevalencesin the study sample were in general equivalent to the population-basedestimates. Therefore, for simplicity of presentation, the resultsfor all subsequent analyses are shown for the study sample alone.
HHV-8 as a Sexually Transmitted Agent
Although HHV-8 infection was strongly associated with sexualorientation, more direct analyses were undertaken to test thehypothesis that HHV-8 is sexually transmitted. First, anti-LANAseropositivity was associated with a history of several sexuallytransmitted diseases (Table 2). It was not associated with severaldiseases that are not believed to be transmitted by intimatesexual contact, such as infectious mononucleosis, asthma, andhay fever. Of particular interest was the association with specificintestinal infections, which in this largely homosexual or bisexualpopulation are probably spread by fecal–oral exposureassociated with sexual activity. Second, there was a linearassociation between the prevalence of anti-LANA antibodies andthe number of male intercourse partners in the previous twoyears (Figure 1). Third, men with more than five years of regularhomosexual intercourse (defined as at least once monthly) hada greater prevalence of HHV-8 infection (213 of 535 men, 39.8percent) than men with between one and five years of regularhomosexual intercourse (7 of 44 men, 15.9 percent), who in turnhad a greater prevalence than men who either had no historyof homosexual intercourse or denied a regular pattern of activity(2 of 197 men, 1.0 percent) (P<0.001 by chi-square test fortrend).
Figure 1. Prevalence of HHV-8 Anti-LANA Antibodies According to the Number of Male Intercourse Partners in the Previous Two Years.
The number of subjects in each group is shown above the bars. P<0.001 by chi-square test for linear trend.
Associations of Potential Risk Factors with HHV-8 Infection
Modes of transmission other than sexual were also examined (Table 3).The univariate association of HHV-8 infection with a historyof transfusion was of borderline statistical significance (P= 0.06). There was a significant univariate association withsharing of needles for recreational-drug use in the previousfive years (P<0.001). Because HIV-related immunocompromisecould conceivably be a risk factor for the acquisition of HHV-8,both HIV infection itself and the absolute CD4 lymphocyte countwere examined, and both were associated with HHV-8 seropositivity(P<0.001 for both).
Table 3. Univariate and Multivariable Logistic-Regression Analyses of the Association between the Prevalence of HHV-8 Anti-LANA Antibodies and Sexual Practices, Injection-Drug Use, History of Transfusion, CD4 Lymphocyte Count, and HIV Serologic Status.
Because all these factors might be confounded by their associationwith a subject's sexual practices, a multivariable logistic-regressionmodel was applied in which each of the factors was adjustedfor the number of male intercourse partners in the previoustwo years, as well as for the other factors in question (Table 3).The association between the number of male intercourse partnersand anti-LANA seropositivity remained very strong. After adjustmentfor the number of sexual partners, the associations with sharingof needles and the CD4 lymphocyte count were no longer significant.The association with HIV infection, however, remained significant.For a history of transfusion, the adjusted odds ratio was notmarkedly changed from the unadjusted estimate, but it was notstatistically significant (odds ratio, 2.30; 95 percent confidenceinterval, 0.80 to 6.63; P = 0.12).
Temporal Associations of HHV-8 Infection with Kaposi's Sarcoma
Ten-year follow-up of the 391 subjects who were HIV-infectedbut free of Kaposi's sarcoma revealed 113 incident cases ofKaposi's sarcoma. At 10 years, 18 of these men (4.6 percent)had been lost to follow-up for ascertainment of Kaposi's sarcoma.No Kaposi's sarcoma was observed in the HIV-uninfected men (includingthose who were infected with HHV-8), and hence they were notincluded in subsequent analyses. Figure 2 shows the Kaplan–Meierestimates of time from enrollment in the cohort to the developmentof Kaposi's sarcoma according to the initial anti-LANA serologicstatus. Base-line anti-LANA seropositivity was significantlyassociated with the subsequent development of Kaposi's sarcoma(relative hazard, 2.40; 95 percent confidence interval, 1.61to 3.58; P<0.001).
Figure 2. Kaplan–Meier Estimates of Time from Study Enrollment to the Development of Kaposi's Sarcoma According to Base-Line HHV-8 Anti-LANA–Antibody Status among 391 HIV-Infected Men.
In the subjects with HHV-8 and HIV infection at base line, themedian time to the development of Kaposi's sarcoma was not quitereached, although the probability of Kaposi's sarcoma at 10years was 49.6 percent (95 percent confidence interval, 41.3to 58.7 percent). After adjustment in a proportional-hazardsregression model for the degree of homosexual activity, as measuredby the number of male intercourse partners in the previous twoyears, as well as for propensity for HIV-related opportunisticdisease, as measured by CD4 count and age, the relative hazardassociated with being anti-LANA–seropositive at base linewas 2.51 (95 percent confidence interval, 1.67 to 3.77; P<0.001),not a substantially altered value. Thus, HHV-8 infection precededand was associated with Kaposi's sarcoma independently of thedegree of sexual activity and HIV-related immunocompromise.
Discussion
In assessing potential causative agents of Kaposi's sarcoma,27,28,29one must ask whether their epidemiology matches that predictedby the epidemiology of Kaposi's sarcoma. That is, the epidemiologyof the candidate agent should probably be that of a sexuallytransmitted agent. We found that HHV-8 seroprevalence was morecommon among homosexual or bisexual men, as did previous studies.8,9,10,11A correlation with sexual orientation, however, is not directproof of sexual transmission. We directly addressed the hypothesisof sexual transmission with information on individual sexualactivity. In addition to being correlated with a history ofsexually transmitted disease and the number of years of regularintercourse with men, HHV-8 infection had a striking independentcorrelation with the number of male intercourse partners. Thisis the most suggestive evidence to date that HHV-8 is sexuallytransmitted.
Sexual exposure was by far the strongest risk factor for HHV-8infection, but surprisingly, the association between HHV-8 infectionand HIV infection remained significant even after adjustmentfor CD4 count. This is most likely explained by some specificsexual practice, not fully captured by the number of sexualpartners, that was associated with the acquisition of both HIVand HHV-8. Alternatively, the association may be explained byclustering of HIV and HHV-8 in those who transmitted the infectionsto these men or by some aspect of HIV infection apart from thedecline in the CD4 cell count that confers host susceptibilityto HHV-8. In the multivariable model, although the odds ratiofor a history of transfusion was not meaningfully altered fromits univariate estimate, history of transfusion was not significantlyassociated with HHV-8 infection. However, transfusion cannotbe excluded as a risk factor, because the confidence intervalstill includes meaningful measures of association. Hence, althoughthe lack of an association with needle sharing might argue againstparenteral transmission, our study cannot draw firm conclusionsabout the role of transfusion.
Base-line anti-LANA reactivity, which indicates HHV-8 infection,preceded and was strongly associated with the subsequent developmentof Kaposi's sarcoma. Although Kaposi's sarcoma did arise inmen whose base-line anti-LANA test was negative, in most ofthese subjects HHV-8 infection almost certainly supervened duringfollow-up. This can be inferred because virtually all patientswith Kaposi's sarcoma are infected with HHV-8 (as judged bypolymerase-chain-reaction [PCR] assay of viral DNA),2,6 andat least 80 percent are anti-LANA–seropositive at or afterdiagnosis.8,9,10 Seroconversion analyses among those who wereinitially anti-LANA–negative are under way. In addition,because of incomplete sensitivity of the anti-LANA assay, somebase-line seronegative results may have been false negatives.Thus, the observed association between base-line HHV-8 infection,as measured by anti-LANA results, and Kaposi's sarcoma probablysubstantially underestimates the true association between HHV-8and the tumor.
Adjustment for the number of male sexual partners as well asthe degree of HIV-related immunocompromise did not alter theassociation between HHV-8 and Kaposi's sarcoma. Adjustment forsexual exposure is particularly important, because it excludesthe possibility that HHV-8 seropositivity might be a markerfor the still undiscovered sexually transmitted agent of Kaposi'ssarcoma.30 Finally, because the study was conducted in a singlegeographic area during a specific period, potential confoundingby regional or temporal differences in HHV-8 prevalence waseliminated. In the absence of an animal model or an unethicalexperimental exposure of humans to HHV-8, this type of well-controlledlongitudinal analysis is likely to yield the strongest evidenceof a causal role of HHV-8 in Kaposi's sarcoma.
The median time from cohort entry to the development of Kaposi'ssarcoma in our subjects coinfected with HIV and HHV-8 was approximately10 years. This is substantially longer than the 3.5 years estimatedby Whitby et al.,13 who measured HHV-8 infection by PCR in peripheral-bloodmononuclear cells. PCR is less sensitive than serologic testsfor the detection of HHV-8 infection10,15 and may be more likelyto detect infection in subjects with a higher viral burden orat a more advanced stage of HHV-8 infection, who may be at riskfor more rapid progression to Kaposi's sarcoma. In addition,the sample size in the study by Whitby et al. (11 subjects)may have contributed to the discrepancy.
Gao et al. also analyzed the median time to the developmentof Kaposi's sarcoma.9,15 They estimated that patients in whomKaposi's sarcoma developed had a median of 3.8 years of precedingHHV-8 infection. This measure is fundamentally different fromours; we estimated the probability that Kaposi's sarcoma woulddevelop in men who were coinfected with HIV and HHV-8 at entryinto the study. These differences in design doubtless contributein important ways to the different estimates. Certainly, shortertimes to the development of Kaposi's sarcoma do occur and willprobably be evident in some initially anti-LANA–seronegativemen in our study in whom HHV-8 infection and Kaposi's sarcomadeveloped during follow-up. Our study, however, clearly showsthat many persons coinfected with HIV and HHV-8 will have muchlonger intervals from HHV-8 infection to the development ofKaposi's sarcoma. Finally, estimates of time to Kaposi's sarcomamade in HIV-infected populations such as ours will probablybe quite different from those in groups without HIV infection.
Because our study intentionally included a large proportionof homosexual and bisexual men, our population-based overallseroprevalence estimate should not be considered representativeof all urban men. Instead, the value of population-based samplingis in the estimates of subpopulation seroprevalences it allows.The seroprevalence of HHV-8 was 37.6 percent in men reportingany homosexual activity and 0 percent in exclusively heterosexualmen. These population-based estimates of HHV-8 seroprevalenceavoid the selection biases associated with samples from clinicsor blood banks or other convenience samples.
Previous work with the anti-LANA assay in a clinic-based populationfound an HHV-8 seroprevalence of 27 percent in homosexual orbisexual men.8 Similar estimates have been obtained with otherserologic assays that measure antibodies to latent-phase viralantigens.9,15 However, because 15 to 20 percent of patientswith Kaposi's sarcoma who have PCR evidence of HHV-8 in theirlesions are seronegative according to these assays, their sensitivityis incomplete. Lennette et al., using an assay designed to detectantibodies to lytic HHV-8 antigens, reported that more than90 percent of homosexual or bisexual men were infected withHHV-8.11 However, subsequent work with lytic antigens in enzymeimmunoassays10,31,32 and indirect immunofluorescent assays33has failed to confirm such a high seroprevalence in homosexualor bisexual men. Regardless of which prevalence estimate iscorrect, characterizing the epidemiology of the anti-LANA–seropositivestate is important. Because we have shown that anti-LANA reactivityis a risk factor for Kaposi's sarcoma, anti-LANA positivitymust mark a special subpopulation of infected persons who areat higher risk for Kaposi's sarcoma, even if HHV-8 is ubiquitousin homosexual and bisexual men.
Understanding the epidemiology of HHV-8 is a critical firststep in designing interventions to decrease the transmissionof this agent. Because many of the risk factors responsiblefor HIV infection probably also increase the risk of HHV-8 infection,many of these prevention efforts have already begun. The potentialtransmission of HHV-8 through unprotected sexual practices providesyet another impetus to reinforce safe sexual behavior.
Supported by individual research awards (R97-SF-034 and R96-SF-142)from the University of California Universitywide AIDS ResearchProgram (to Drs. Martin, Osmond, and Kedes) and by a traininggrant (T32 MH-19105) from the National Institutes of Health(to Dr. Martin).
Source Information
From the Center for AIDS Prevention Studies (J.N.M., D.H.O., K.A.P.-S.), the Department of Epidemiology and Biostatistics (J.N.M., D.H.O.), and the AIDS Program and Infectious Diseases Division (J.N.M.), Department of Medicine, San Francisco General Hospital, San Francisco; and the Howard Hughes Medical Institute (D.E.G., D.M.), the Department of Medicine (D.E.G.), and the Department of Microbiology and Immunology (D.E.G., D.H.K.), University of California, San Francisco.
Address reprint requests to Dr. Kedes at the Department of Microbiology and Immunology, Box 0414, University of California, San Francisco, San Francisco, CA 94143-0414.
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