Antibodies to Butyrate-Inducible Antigens of Kaposi's Sarcoma–Associated Herpesvirus in Patients with HIV-1 Infection
George Miller, M.D., Michael O. Rigsby, M.D., Lee Heston, M.S., Elizabeth Grogan, B.S., Ren Sun, Ph.D., Craig Metroka, M.D., Ph.D., Jay A. Levy, M.D., Shou-Jiang Gao, Ph.D., Yuan Chang, M.D., and Patrick Moore, M.D., M.P.H.
Background The recent identification in patients with Kaposi'ssarcoma of DNA sequences with homology to gammaherpesviruseshas led to the hypothesis that a newly identified virus, Kaposi'ssarcoma–associated herpeslike virus (KSHV), has a rolein the pathogenesis of Kaposi's sarcoma. We developed serologicmarkers for KSHV infection.
Methods KSHV antigens were prepared from a cell line (BC-1)that contains the genomes of both KSHV and the Epstein–Barrvirus (EBV). We used immunoblot and immunofluorescence assaysto examine serum samples from 102 patients with human immunodeficiencyvirus type 1 (HIV-1) infection for antibodies to KSHV-associatedproteins and to distinguish these antibodies from antibodiesto EBV antigens. A positive serologic response was defined bythe recognition of an antigenic polypeptide, p40, in n-butyrate–treatedBC-1 cells and by the absence of p40 recognition in untreatedBC-1 cells or EBV-infected, KSHV-negative cells. The detectionby the immunofluorescence assay of 10 to 20 times more antigen-positivecells in n-butyrate–treated BC-1 cells than in untreatedcells was considered a positive response.
Results Antibodies to the p40 antigen expressed by chemicallytreated BC-1 cells were identified in 32 of 48 HIV-1–infectedpatients with Kaposi's sarcoma (67 percent), as compared withonly 7 of 54 HIV-1–infected patients without Kaposi'ssarcoma (13 percent). These results were confirmed by an immunofluorescenceassay. The positive predictive value of the serologic testsfor Kaposi's sarcoma was 82 percent, and the negative predictivevalue 75 percent.
Conclusions The presence of antibodies to a KSHV antigenic peptidecorrelates with the presence of Kaposi's sarcoma in a high-riskpopulation and provides further evidence of an etiologic rolefor KSHV.
Kaposi's sarcoma, a multifocal vascular tumor, was first describedby the Hungarian-born dermatologist Moritz Kaposi in 1872.1The classic form predominantly affects men of Eastern Europeanand Mediterranean heritage.2 Kaposi's sarcoma also occurs inimmunocompromised patients, particularly homosexual and bisexualmen with human immunodeficiency virus type 1 (HIV-1) infectionand allograft recipients receiving immunosuppressive therapy.3,4,5,6,7An endemic form that does not involve HIV is found in centralAfrica.8
The possibility that an infectious agent is involved in thepathogenesis of Kaposi's sarcoma is suggested by the clusteringof the disease in well-defined populations and the relationof the disease to immunosuppression. Several agents have beeninvestigated as etiologic factors, including cytomegalovirus,the human papillomavirus, and Mycoplasma penetrans.9,10,11,12,13,14Recently, Chang et al. found novel DNA sequences with substantialsequence homology to the gammaherpesviruses Epstein–Barrvirus (EBV) and herpesvirus saimiri in Kaposi's sarcoma lesions.15,16The putative new herpesvirus has been designated Kaposi's sarcoma–associatedherpeslike virus (KSHV). KSHV sequences have been detected intissue from more than 90 percent of HIV-1–associated Kaposi'ssarcoma lesions, as well as in biopsy specimens from patientswith classic Kaposi's sarcoma, endemic Kaposi's sarcoma, andpost-transplantation Kaposi's sarcoma.17,18,19,20,21,22,23 Twolymphoproliferative disorders related to the acquired immunodeficiencysyndrome (AIDS) — body-cavity–based lymphomas24and multicentric Castleman's disease25 — have also beenlinked to KSHV by the detection of KSHV sequences in the tumors.
To facilitate further investigation of the relation betweenKSHV and the pathogenesis of Kaposi's sarcoma, we have developedserologic assays for KSHV infection. The development of theseassays relied on the capacity of sodium butyrate, an agent knownto trigger transcription from silent cellular and viral genes,26,27,28to activate the expression of the KSHV genome in a KSHV-infectedcell line.
Methods
Patients
Serum was collected from a convenience sample of 48 patientswith AIDS and Kaposi's sarcoma and 54 HIV-1–infected controlpatients at several clinical sites in Connecticut, New York,and California. Demographic and clinical information about thepatients was recorded on standardized forms that were linkedto the samples by a numerical code. Ninety-nine of the 102 patients(97 percent) were men; 92 patients (90 percent) were homosexualor bisexual (Table 1). In 46 patients the diagnosis of Kaposi'ssarcoma was histologically confirmed; in the remaining 2 thediagnosis was unequivocal on clinical grounds.
The BC-1 cell line was established from an AIDS-associated body-cavityB-cell lymphoma.29,30 KSHV DNA sequences can be detected inBC-1 cells by DNA hybridization with KS330Bam and KS631Bam,probes originally generated by representational difference analysis.15,31BC-1 cells also contain an EBV genome that is detectable withseveral EBV DNA probes.30 B95-8 is an EBV-producing marmosetcell line that can be efficiently induced to express the EBVlytic-cycle gene by phorbol esters (12-O-tetradecanoylphorbol-13acetate [TPA]).32,33 HH514-16 is an EBV-containing cell clone,originally from a Burkitt's lymphoma, that can optimally beinduced to express the EBV lytic-cycle gene by sodium butyrate.28,34BL41 is an EBV-negative Burkitt's lymphoma cell line.35 B95-8,HH514-16, and BL41 do not hybridize with the KSHV probes (datanot shown). All the cell lines were cultured in RPMI 1640 mediumcontaining 8 to 15 percent fetal-calf serum.
Immunoblot Assays
Extracts of untreated BC-1 cells and of cells treated for 48hours with 20 ng of TPA (Calbiochem) per milliliter, 3 mM n-butyricacid, sodium salt (Sigma), or a mixture of these inducing chemicalswere prepared by sonication. HH514-16 cells, treated similarly,served to control for antibody reactivity to EBV polypeptides.Each lane of 10 or 12 percent polyacrylamide gel was loadedwith an extract of 250,000 cells in sodium dodecyl sulfate samplebuffer; electrophoresis, transfer to nitrocellulose, and blockingwith skim milk followed standard protocols.36 Serum sampleswere screened at a dilution of 1:100. Antigen–antibodyreactions were detected by the addition of 1.0 µCi ofstaphylococcal protein A labeled with iodine-125 (Amersham),and the radioautographs were exposed to film for 24 to 48 hours.The immunoblotting assays were performed and interpreted whilethe serum samples remained coded.
Immunofluorescence Assay
The antigens sought were present in BC-1 cells that were eitheruntreated or treated with 3 mM n-butyrate for 48 hours. Thecells were dropped onto slides that were subsequently fixedin acetone and methanol. Serum samples were tested at a dilutionof 1:10, followed by a 1:30 dilution of fluorescein sheep antihumanimmunoglobulin (Wellcome). The reactivity of a serum samplewith untreated BC-1 cells and its reactivity with n-butyrate–treatedcells were compared. When several serum samples were used, 0.5to 2.0 percent of untreated BC-1 cells were antigen-positive.When there was reactivity with 10 to 20 times more n-butyrate–treatedBC-1 cells than untreated cells, the reaction was consideredto be positive. Serum samples containing antibodies to EBV butnot to KSHV recognized the same number of antigen-positive cellsin both untreated and n-butyrate–treated preparations.All the immunofluorescence tests were performed on coded serumsamples, and the results were interpreted by readers unawareof the patients' disease status or the results of the immunoblotassays.
Results
Chemical Induction of KSHV-Associated Proteins in BC-1 Cells
Because serum samples from an HIV-1–infected patient wouldbe expected to contain antibodies to EBV polypeptides whetheror not the patient had Kaposi's sarcoma and because BC-1 cellsare dually infected with KSHV and EBV, it was essential to distinguishEBV polypeptides from polypeptides encoded or induced by KSHV.The technique of immunoblotting was used to determine whetherthe BC-1 cells expressed antigenic polypeptides specific forKSHV infection. Figure 1A shows that BC-1 cells expressed atleast two EBV polypeptides, representing the latent nuclearantigen EBNA-1 and p21, a late capsid-antigen complex,37 thatwere also present in other EBV-producer cell lines, such asB95-8 (Figure 1A) and HH514-16 (Figure 1B, Figure 2A), and Figure 2B).When serum samples from patients with Kaposi's sarcomawere used as a source of antibody in immunoblot reactions withextracts from untreated BC-1 cells, they did not identify additionalantigenic polypeptides that were not also seen in the EBV-producercell lines. However, when extracts were prepared from BC-1 cellsthat were first treated with a combination of TPA and n-butyrate,serum from patients with Kaposi's sarcoma recognized a numberof novel polypeptides that were present in the BC-1 cell linebut not in the EBV-producer cell lines (Figure 1B, Figure 2A),and Figure 2B). The molecular weights of the most prominentof these many polypeptides were estimated at 27,000, 40,000,and 60,000 on 10 percent polyacrylamide gels. These polypeptideswere detected within 24 hours after the addition of the inducingagents. Since p27, p40, and p60 were not detected in the untreatedcells and appeared after the treatment with chemicals, theywere thought likely to represent lytic-cycle rather than latent-cyclepolypeptides of KSHV. Further experiments showed that n-butyratewas the chemical agent primarily responsible for the inductionof p40 (Figure 2A) and Figure 2B).
Figure 1. Immunoblots Demonstrating the Specific Recognition of KSHV Polypeptides in Chemically Treated BC-1 Cells.
Panel A shows the reactivity of untreated BC-1 cells (from a cell line established from an AIDS-associated body-cavity B-cell lymphoma) and B95-8 cells with a 1:200 dilution of a reference human antibody to EBV. The reference antibody recognizes the EBV polypeptides EBNA-1 and p21 in the BC-1 cells. Panel B shows the reactivity of various untreated and chemically treated cell lines with a 1:400 dilution of serum from a patient with Kaposi's sarcoma. The cells were treated for 48 hours with 12-O-tetradecanoylphorbol-13 acetate (TPA) and n-butyrate. The serum tested in Panel B recognizes many antigenic polypeptides in the treated BC-1 cells. For a description of the cell lines, see the Methods section. The immunoblots were prepared from 10 percent sodium dodecyl sulfate–poly-acrylamide gels.
Figure 2. Immunoblots Showing the Detection of KSHV p40 by Antiserum from Patients with Kaposi's sarcoma.
Extracts were prepared from BC-1 cells (containing KSHV and EBV) and cloned HH514-16 cells (containing only EBV) that were either untreated or treated chemically for 48 hours with n-butyrate, 12-O-tetradecanoylphorbol-13 acetate (TPA), or both. Panels A and B show the reactivity of immunoblots prepared from 12 percent sodium dodecyl sulfate–polyacrylamide gels with 1:200 dilutions of serum from two HIV-1–positive patients with Kaposi's sarcoma.
Specificity of p40 for KSHV
Figure 1B, Figure 2A), and Figure 2B show that no antigenicpolypeptides corresponding in molecular weight to p40 were observedin two EBV-producer lines, B95-8 and HH514-16, when the EBVlytic cycle was induced by the same chemicals. Nor was p40 detectedin similarly treated, EBV-negative BL41 cells. Many serum samplesfrom patients with Kaposi's sarcoma still recognized KSHV-associatedp40 when they were diluted so that they no longer reacted withEBV polypeptides (data not shown). Furthermore, n-butyrate stronglyinduced the expression of p40 in BC-1 cells but had little orno effect on the level of expression of the EBV early or lateantigens in the same cells, which were detected with monospecificantibodies to EBV gene products. Thus, the presence of p40 appearedto represent specific expression of the KSHV genome in the chemicallyinduced BC-1 cells. In related experiments, we have found thatn-butyrate treatment also increased the abundance of KSHV DNAand KSHV late lytic-cycle messenger RNA (mRNA) but had littleor no effect on the content of EBV DNA or EBV late-cycle mRNA(data not shown). TPA, by contrast, induced the EBV lytic cyclein BC-1 cells efficiently; treatment with TPA increased theabundance of EBV DNA but caused only minimal induction of KSHVDNA.38 These findings suggested that the switch of the two gammaherpesvirusescarried by BC-1 cells from the latent to the lytic cycle wasunder separate control and provided further evidence that thep40 complex observed after n-butyrate treatment was specificto the KSHV genome.
Studies of P40 as a Serologic Marker for KSHV
Although a few highly reactive serum samples from patients withKaposi's sarcoma, such as the one used in Figure 1B, recognizedmultiple antigenic proteins unique to the chemically treatedBC-1 cells, including p27, p40, and p60, serum from other patientswith Kaposi's sarcoma did not react with p27 or p60 but didrecognize p40 (Figure 2B). Therefore, recognition of p40 wasstudied as a serologic marker for infection with KSHV. Serumsamples from the 102 HIV-1–infected patients were examinedfor the presence of antibodies against p40 (Table 2). Thirty-twoof the 48 patients with Kaposi's sarcoma (67 percent) had suchantibodies, as compared with only 7 of the 54 patients withoutKaposi's sarcoma (13 percent, P<0.001 by the chi-square test).These seven patients were homosexual or bisexual men from NewYork City or San Francisco. None of the 13 HIV-positive patientswithout Kaposi's sarcoma from Connecticut had serum containingp40 antibodies. The positive and negative predictive valuesof this serologic marker for the presence of Kaposi's sarcomawere 82 percent and 75 percent, respectively. The patients withKaposi's sarcoma who did not have p40 antibodies did not differfrom those with p40 antibodies with regard to demographic orHIV-related variables (Table 3).
Table 3. Characteristics of Patients with Kaposi's Sarcoma, According to p40 Status.
Immunofluorescence Assays
Immunoblot assays showed that n-butyrate induced the expressionof KSHV lytic-cycle polypeptides in BC-1 cells without substantiallyaffecting the expression of EBV polypeptides (Figure 1B, Figure 2A,and Figure 2B, and unpublished data). Therefore, we reasonedthat n-butyrate might also induce many more BC-1 cells to switchinto the KSHV replicative cycle than into the EBV lytic cycle.When we performed indirect immunofluorescence assays with areference human antiserum that contained antibodies to EBV butnot to KSHV (Figure 1A), 2 percent of cells in the untreatedBC-1 line were antigen-positive, as were a similar percentageof the BC-1 cells treated with n-butyrate. The use of serumthat was EBV-positive and highly reactive to KSHV antigens (Figure 1B)identified 2 percent of cells in the untreated BC-1 populationas antigen-positive, presumably the EBV-expressing cells, whereas30 to 50 percent of the BC-1 cells treated with n-butyrate wereshown to be antigen-positive. The antigens detected were foundmainly in the cytoplasm and on the cytoplasmic membrane (Figure 3).This increased number of antigen-positive BC-1 cells inthe n-butyrate–treated population served as the basisof an immunofluorescence assay to screen for antibodies to inducibleKSHV antigens.
Figure 3. Detection of KSHV Lytic-Cycle Antigens by an Indirect Immunofluorescence Assay.BC-1 cells were either untreated (left-hand panels) or treated with n -butyrate for 48 hours (right-hand panels). Indirect immunofluorescence assays were performed with 1:10 dilutions of serum from each of two patients with Kaposi's sarcoma (top and bottom panels) and serum from a control patient without Kaposi's sarcoma (middle panels).
The results of the immunofluorescence assay were nearly identicalto those of the immunoblot assay (Table 2). Sixty-five percentof patients with Kaposi's sarcoma and 13 percent of HIV-1–infectedpatients without Kaposi's sarcoma had serum reactive by theimmunofluorescence assay. Only 3 of the 102 serum samples tested(3 percent) yielded discordant results on the two assays. Oneserum sample scored positive by the immunofluorescence assayand negative by the immunoblot assay; two were considered positiveby the immunoblot assay and negative by the immunofluorescenceassay.
The odds ratios for the association of these antibodies withKaposi's sarcoma were 13.4 (95 percent confidence interval,4.5 to 42) for the immunoblot assay and 12.2 (95 percent confidenceinterval, 4.1 to 38) for the immunofluorescence assay. The predictivevalue of a positive test for antibodies by either assay was82 percent. Thus, the presence of antibodies in the serum ofHIV-1–infected persons to chemically induced KSHV-associatedantigens was strongly correlated with the clinical presenceof Kaposi's sarcoma.
Discussion
The recent discovery of genetic sequences representative ofa new human herpesvirus in Kaposi's sarcoma tissue, togetherwith past epidemiologic observations, strongly implicates thisnovel agent in the pathogenesis of Kaposi's sarcoma. However,these observations in themselves do not permit the constructionof a unified theory of pathogenesis that accounts for the manyunexplained features of Kaposi's sarcoma. Because it would allowthe infection rate in various populations to be identified,a serologic marker for infection with KSHV would be a greataid in determining the role of the new virus.
Our findings, using tests for antibodies to chemically inducedKSHV antigens, are most consistent with a model in which KSHVinfection is infrequent but is associated with a high rate ofclinically apparent disease. Only 13 percent of HIV-1–infectedpatients without Kaposi's sarcoma had antibodies to the KSHVantigen; by contrast, a very large proportion of HIV-1–infectedmen with clinically evident Kaposi's sarcoma were seropositive.Further evidence for low rates of seroreactivity in patientswithout Kaposi's sarcoma has been provided by Moore et al. instudies of HBL-6 cells, another KSHV- and EBV-infected cellline.38 Using serum samples from HIV-1–infected patients,they found that mean antibody titers to uninduced HBL-6 cellswere nine times higher in 14 patients with Kaposi's sarcomathan in 16 patients without Kaposi's sarcoma.
Another possible interpretation of our data is that KSHV infectionmay be ubiquitous, but that antibodies to n-butyrate–inducedviral antigens are not normally detectable in healthy infectedpersons. These antibodies might appear only after the virushas been reactivated from the latent into the lytic cycle, asmight occur in the course of immunosuppression. Thus, our serologictests might detect markers of reactivated infection but notof past exposure to the virus. If this interpretation is correct,it should be possible to demonstrate KSHV DNA sequences or toisolate the virus from healthy persons whose serum is nonreactive,either to p40 antigen or by the immunofluorescence assay.
In our study, seven patients had positive serologic tests butno clinical evidence of Kaposi's sarcoma. They were all homosexualmen from New York City or San Francisco, cities whose populationsare at higher risk for Kaposi's sarcoma than the general NorthAmerican population.7 Kaposi's sarcoma subsequently developedin two of the patients from New York; one had gastrointestinalinvolvement, and the other cutaneous lesions. Possibly the viscerallesions were present at the time of the initial evaluation.
Approximately 30 percent of the patients with Kaposi's sarcomahad no demonstrable seroreactivity in our assays. Several explanationsfor this are possible. The p40 antigen may not be abundant ormay be only weakly antigenic in some patients. If antibody top40 indicates the extent of lytic KSHV replication, the appearanceof these antibodies may vary in different phases of the disease.It is unlikely that these patients were not infected with KSHV,since the genetic sequences are nearly universal in Kaposi'ssarcoma lesions.25 In a separate study, KSHV sequences wereidentified in peripheral-blood mononuclear cells, Kaposi's sarcomatissue, or both from three of the KSHV-seronegative patientsfrom California who had Kaposi's sarcoma.20
The p40 antigen is likely to be only one of a number of KSHVantigens that are recognized by the serum of infected patients.Antibody recognition of other KSHV antigens may be impossibleon immunoblot assays for several reasons: because the antigenscomigrate with EBV polypeptides, because BC-1 cells cannot beinduced to express these antigens, or because the antigens arenot abundant or are denatured on the immunoblots. These testsusing whole BC-1 cells as antigen are clearly first-generationassays, to be improved by better characterization of the KSHVgene products and by the preparation of recombinant antigens.
In summary, we describe immunoblot and immunofluorescence screeningassays to detect antibodies to n-butyrate–induced antigensthat are likely to represent lytic-cycle gene products of KSHV.Our findings support the hypothesis of a strong associationbetween KSHV infection, as defined by the presence of antibodiesto the inducible antigens, and clinically evident Kaposi's sarcomain HIV-1–infected patients.
Supported by grants (AI 22959 and CA 70036) from the NationalInstitutes of Health (to Dr. Miller) and by a grant (R95-SF-088)from the state of California (to Dr. Levy).
We are indebted to Drs. Gary Blick, Helena Brett-Smith, andLeonard Farber for their assistance in identifying patientsand providing serum samples.
Source Information
From the Departments of Pediatrics (G.M., L.H., E.G.), Internal Medicine (M.O.R.), Epidemiology and Public Health (G.M.), Molecular Biophysics and Biochemistry (G.M., R.S.), and Genetics (R.S.), Yale University School of Medicine, New Haven, Conn.; St. Luke's–Roosevelt Hospital Center, New York (C.M.); the University of California, San Francisco, School of Medicine, San Francisco (J.A.L.); and the College of Physicians and Surgeons and School of Public Health, Columbia University, New York (C.M., S.-J.G., Y.C., P.M.).
Address reprint requests to Dr. Miller at the Department of Pediatrics, Yale University School of Medicine, 333 Cedar St., Rm. 420 LSOG, New Haven, CT 06520.
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