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Results for “Viral Structures”

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PubMed2005

Complete genome sequence of the grouper iridovirus and comparison of genomic organization with those of other iridoviruses.

The complete DNA sequence of grouper iridovirus (GIV) was determined using a whole-genome shotgun approach on virion DNA. The circular form genome was 139,793 bp in length with a 49% G + C content. It contained 120 predicted open reading frames (ORFs) with coding capacities ranging from 62 to 1,268 amino acids. A total of 21% (25 of 120) of GIV ORFs are conserved in the other five sequenced iridovirus genomes, including DNA replication, transcription, nucleotide metabolism, protein modification, viral structure, and virus-host interaction genes. The whole-genome nucleotide pairwise comparison showed that GIV virus was partially colinear with counterparts of previously sequenced ranaviruses (ATV and TFV). Besides, sequence analysis revealed that GIV possesses several unique features which are different from those of other complete sequenced iridovirus genomes: (i) GIV is the first ranavirus-like virus which has been sequenced completely and which infects fish other than amphibians, (ii) GIV is the only vertebrate iridovirus without CpG sequence methylation and lacking DNA methyltransferase, (iii) GIV contains a purine nucleoside phosphorylase gene which is not found in other iridoviruses or in any other viruses, (iv) GIV contains 17 sets of repeat sequence, with basic unit sizes ranging from 9 to 63 bp, dispersed throughout the whole genome. These distinctive features of GIV further extend our understanding of molecular events taking place between ranavirus and its hosts and the iridovirus evolution.

Animals↗

PubMed2001

Papillomavirus-like particles induce acute activation of dendritic cells.

The role of viral structural proteins in the initiation of adaptive immune responses is poorly understood. To address this issue, we focused on the effect of noninfectious papillomavirus-like particles (VLPs) on dendritic cell (DC) activation. We found that murine bone marrow-derived dendritic cells (BMDCs) effectively bound and rapidly internalized bovine papillomavirus VLPS: Exposure to fully assembled VLPs of bovine papillomavirus, human papillomavirus (HPV)16 or HPV18, but not to predominately disordered HPV16 capsomers, induced acute phenotypic maturation of BMDCS: Structurally similar polyomavirus VLPs bound to the DC surface and were internalized, but failed to induce maturation. DCs that had incorporated HPV16 VLPs produced proinflammatory cytokines IL-6 and TNF-alpha; however, the release of these cytokines was delayed relative to LPS activation. Production of IL-12p70 by VLP-exposed DCs required the addition of syngeneic T cells or rIFN-gamma. Finally, BMDCs pulsed with HPV16 VLPs induced Th1-dominated primary T cell responses in vitro. Our data provide evidence that DCs respond to intact papillomavirus capsids and that they play a central role in VLP-induced immunity. These results offer a mechanistic explanation for the striking ability of papillomavirus VLP-based vaccines to induce potent T and B cell responses even in the absence of adjuvant.

Animals↗

PubMed1996

Expression of additional genes in a vector derived from a minimal RNA virus.

Previous studies have shown that expression of the vesicular stomatitis virus (VSV) glycoprotein (G) from a Semliki Forest virus (SFV) RNA replicon results in the production of propagating infectious particles that we call minimal viruses. These minimal viruses consist of vesicles containing VSV G protein that bud from the plasma membrane and trap the infectious SFV G RNA, but they do not contain other viral structural proteins. The cell binding and membrane fusion activity of the VSV G protein allow minimal viruses to propagate in tissue culture cells. To determine if these minimal viruses could be used to express foreign genes, we added a second SFV promoter and a multiple cloning site downstream of the VSV G gene. We report here expression of three different proteins from this modified, minimal virus vector. Although expression of each foreign, unselected gene was lost rapidly from the vector upon passaging, it was possible after the initial transfection to derive stocks of infectious particles that could be used to infect multiple additional cultures and transfer protein expression efficiently. When cells were infected with these minimal viruses, host protein synthesis was shut off and the foreign protein and VSV G proteins were the major proteins expressed in the infected cells. Both were expressed at similar levels and accumulated to about 1-2% of total cell protein.

Animals↗

PubMed1996

Identification and characterization of a small modular domain in the herpes simplex virus host shutoff protein sufficient for interaction with VP16.

The herpes simplex virus transactivator VP16 and the virion host shutoff protein vhs are viral structural components that direct the activation of immediate-early gene expression and the arrest of host protein synthesis, respectively, during an infection. Recent studies show that VP16 and vhs physically interact with each other in vitro and in infected cells, suggesting that their respective regulatory functions are coupled. In this report, we used the yeast two-hybrid system and affinity chromatography with purified VP16 fusion proteins to precisely map a region in vhs that directs interaction with VP16. Deletion analysis of vhs demonstrated that a 21-amino-acid-long domain spanning residues 310 to 330 (PAAGGTEMRVSWTEILTQQIA) was sufficient for directing complex formation with VP16 in vivo and in vitro when fused to a heterologous protein. Site-directed mutagenesis of this region identified tryptophan 321 as a crucial determinant for interaction with VP16 in vitro and in vivo and additional residues that are important for stable complex formation in vitro. These findings indicate that vhs residues 310 to 330 constitute an independent and modular binding interface that is recognized by VP16.

Amino Acid Sequence↗

PubMed1991

Avian cells expressing the murine Mx1 protein are resistant to influenza virus infection.

The cDNA encoding the murine Mx1 protein, a mediator of resistance to influenza virus, was inserted into a replication-competent avian retroviral vector in either the sense (referred to as Mx+) or the antisense (referred to as Mx-) orientation relative to the viral structural genes. Both vectors produced virus retaining the Mx insert (Mx recombinant viruses referred to as Mx+ and Mx-) following transfection into chicken embryo fibroblasts (CEF). Mx protein of the appropriate size and nuclear localization was expressed only in CEF cells infected with the Mx+ virus. Mx expression was observed in all Mx(+)-infected cells and was stable during long-term culture. Cells infected with the Mx+ virus were resistant to infection by human influenza A/WSN/33 (H1N1) and avian influenza viruses A/Turkey/Wisconsin/68 (H5N9) and A/Turkey/Massachusetts/65 (H6N2), but were susceptible to infection by the enveloped RNA viruses Sindbis and vesicular stomatitis virus (VSV). Normal CEF and cells infected with the Mx virus were susceptible to influenza A, Sindbis, and VSV. The synthesis of influenza proteins, especially the larger polymerase and hemagglutinin proteins, was reduced in Mx+ retrovirus-infected cells superinfected by influenza A.

Animals↗

PubMed2002

Analysis of intratypic variation evident in an Ibaraki virus strain and its epizootic hemorrhagic disease virus serogroup.

A new strain of Ibaraki virus (IBAV) was isolated from cattle showing atypical symptoms of Ibaraki disease. The isolate was genetically characterized, and the genetic diversity and evolution of the capsid proteins of viruses in the epizootic hemorrhagic disease virus (EHDV) serogroup were investigated. The nucleotide sequences of the isolate's viral RNA segments 2, 3, 6, and 7, which encode the viral structural proteins VP2, VP3, VP5, and VP7, respectively, were determined and were then compared against those of the existing strains of IBAV and EHDV, to which IBAV belongs serologically. The nucleotide sequences of segments 3 and 7 were conserved within the EHDV serogroup, particularly well among the strains of IBAV and Australian EHDV. The similarity of the sequence of segment 6 of the isolate to sequences of corresponding segments of the other strains of IBAV and EHDV was found to be about 93%. The similarity of segment 2 of the isolate to segments 2 of the other strains of IBAV and EHDV was less than 70%. Phylogenetic analysis based on the deduced amino acid sequences of segments 3 and 7 revealed that the viruses differed according to their geographical distributions. However, the new isolate of IBAV was categorized as having a distinct lineage in the phylogenetic tree of VP2. These results suggest that the isolate was modified by a reassortment of segment 2 and that it exhibits unique genetic and antigenic characteristics.

Animals↗

PubMed2000

"Ambisense" approach for the generation of influenza A virus: vRNA and mRNA synthesis from one template.

We present a system for creating influenza virus by generating viral RNA (vRNA) and mRNA from one template. Recently, a system for the generation of influenza A virus entirely from cloned cDNAs was established (Neumann et al., 1999, Proc. Natl. Acad. Sci. USA 96, 9345-9350). Cells were transfected with plasmids for RNA polymerase I-driven intracellular synthesis of all eight viral RNAs, and with protein expression plasmids for the synthesis of viral structural proteins. Although this system is highly efficient in virus generation, the construction and cotransfection of 17 plasmids is cumbersome and may limit the use of this system to cell lines that can be transfected with high efficiencies. Synthesizing both vRNA and mRNA from one template would reduce the number of plasmids required for virus generation. Therefore, we generated a bidirectional transcription construct that contains cDNA encoding PB1 flanked by an RNA polymerase I (pol I) promoter for vRNA synthesis and an RNA polymerase II (pol II) promoter for mRNA synthesis. The utility of this approach is proved by the generation of virus after transfecting the pol I/pol II-promoter-PB1 construct together with vRNA- and protein-expression constructs for the remaining seven segments. Because this approach reduces the number of plasmids required for virus generation, it also reduces the work necessary for cloning, probably enhances the efficiency of virus generation, and expands the use of the reverse-genetics system to cell lines for which efficient cotransfection of 17 plasmids cannot be achieved.

Animals↗

PubMed1997

Immunological reactivity of baculovirus-expressed enterovirus proteins.

In order to study immunological reactivity of individual enterovirus polypeptides and evaluate their usefulness for enterovirus diagnosis, the genes coding for viral structural and nonstructural proteins were expressed using recombinant baculoviruses. A histidine-tailed coxsackievirus B3 (CBV3) VP1 capsid protein was expressed and purified by immobilized metal ion affinity chromatography for EIAs. To elucidate the usefulness of the other CBV3 capsid proteins for immunoassays, recombinant baculovirus expressing the whole CBV3 capsid polyprotein region was constructed. For the detection of a potentially broader spectrum of enteroviruses, the conserved nonstructural P3 region was expressed. The P3 region encodes four nonstructural proteins including a cysteine protease (3C) and an RNA-dependent RNA-polymerase (3D). The 3C polypeptide was shown to be proteolytically active indicating that the baculovirus system is capable of expressing biologically functional enterovirus proteins. Immunoblot analysis detected antibodies against the VP1, 3C and 3D proteins in human serum samples. When the baculovirus-expressed antigens were compared with lysates of enterovirus-infected cells and a synthetic peptide in EIA highly similar results were obtained with recombinant VP1 and the lysate antigens. Although reactive in immunoblots, the P3 encoded proteins were not satisfactory for EIA.

Baculoviridae↗

PubMed2002

An ELISA for antibodies against infectious bronchitis virus using an S1 spike polypeptide.

Using the whole infectious bronchitis virus (IBV) for detecting the antibody against IBV by enzyme-linked immunosorbent assay (ELISA) is a routine work in poultry industry. To prepare virus is time consuming and tedious. Furthermore, the whole viral antigen detects all antibodies against the viral structural proteins, including spike (S), nucleocapsid, matrix, and other proteins. Among those, S protein is related to neutralization. Thus, to develop and express protein fragment from S gene and to use the protein as a coating antigen for antibody detection against IBV are the purposes of this experiment. A partial S gene fragment (n.t. 1143-1665) was cloned into pRSET vectors and transformed into competent Escherichia coli (E. coli) BL21 (DE3). A 27.5 kDa fusion protein (S-fg, containing S1-F and partial S2-G antigenic sites) was successfully expressed, affinity-purified and detected specifically with chicken anti-IBV serum by Western blot. The expressed S-fg protein was used as a coating antigen for developing an ELISA (S-fg ELISA) for serum antibody detection in anti-IBV antisera from different IBV serotypes and in field sera. The results show that the S-fg fusion protein is highly cross-reactive among different IBV serotypes, and the S-fg ELISA is found to be a convenient, economical, and efficient method for antibody detection against IBV.

Animals↗

PubMed1989

Lymphocyte subpopulations in sheep during the early stage of experimental infection with bovine leukaemia virus.

Sheep were experimentally infected with bovine leukaemia virus (BLV) by the inoculation of PBL from leukaemic sheep. Antibodies to viral structural proteins were detected at from 2 to 6 weeks after inoculation. At seroconversion, all sheep had a marked increase in the number of circulating lymphocytes, due essentially to an increase in the number of B cells. The number of circulating B cells then decreased but remained higher than pre-infection levels. A second increase in this population preceded the development of a B cell lymphoblastic leukaemia. Generalized lymphosarcoma was diagnosed at necropsy of all sheep. Variation between individual sheep in the time from infection to the development of tumours allowed two clearly delineated groups of nine sheep to be compared. A study of changes in the B cell and T cell populations during the first 16 weeks of infection suggested that the initial response to infection influences the subsequent rate of leukaemogenesis. At seroconversion the number of circulating B cells was significantly higher in group 1 (10.16 +/- 1.51 X 10(9)/l) than in group 2 (6.47 +/- 2.76 X 10(9)/l). Group 1 sheep became leukaemic at 20-50 weeks after infection, whereas group 2 sheep did not do so until 70-95 weeks after infection.

Animals↗

PubMed1989

Characterization of Japanese encephalitis virus envelope protein expressed by recombinant baculoviruses.

Recombinant baculoviruses containing the coding sequences of the viral structural proteins, i.e., the capsid (C) protein, the precursor to premembrane (preM) protein, and the envelope (E) protein, as well as a nonstructural protein, NS1, of Japanese encephalitis virus (JEV) were constructed. Infection of Spodoptera frugiperda cells with these recombinant viruses produced PreM and E proteins. The E proteins synthesized by the recombinants were shown to be glycosylated and similar in size to the authentic E protein. The E protein was found on the surface of infected cells. The antigenic properties of recombinant E proteins were evaluated using a panel of monoclonal antibodies produced against JEV E protein. It was demonstrated that all of the epitopes detectable on the authentic JEV E protein were present on the recombinant E protein expressed by a recombinant baculovirus containing the coding sequence for a part of C, PreM, E, and a part of NS1 proteins. However, for E protein expressed by a recombinant baculovirus having the coding sequence of only a part of PreM, but all of E and a part of NS1, one of the flavivirus cross-reactive epitopes was not detected. Mice immunized with cells infected with the recombinant baculoviruses developed neutralization antibodies.

Animals↗

PubMed2006

[Application of nucleic acid sequence-based amplification in detection of cytomegalovirus mRNA of recipients after allogeneic peripheral blood stem cell transplantation].

The study was purposed to investigate diagnostic value of late-mRNA detection by nucleic acid sequence-based amplification (NASBA) technique for human cytomegalovirus (HCMV) infection of the recipients after allogeneic peripheral blood stem cell transplantation (allo-PBSCT) and to evaluate the clinical significance for guiding antiviral therapy. 352 samples were collected from 128 transplant patients after allo-PBSCT. A molecular biological diagnostic technique--NASBA was used to detect human cytomegalovirus (HCMV) late mRNA encoding the viral structural protein PP67 (UL65) expression in peripheral blood of recipients after allo-PBSCT, and the detected results were compared with HCMV DNA detection by PCR. The sensitivity, specificity and early diagnostic value of HCMV mRNA detection for HCMV disease were evaluated. The results showed that out of 352 detected blood specimens from 84 patients 183 specimens (51.99%) were positive of HCMV DNA by PCR, 105 specimens (29.83%) were positive of HCMV mRNA by NASBA. 45 patients were infected by HCMV. The sensitivity and specificity of HCMV DNA and HCMV mRNA for detecting HCMV disease were 95.56% (43/45), 93.33% (42/45) and 60.24% (50/83), 97.59% (81/83). The results of specificity showed significant difference between two groups of HCMV mRNA and HCMV DNA (P < 0.05). It is concluded that the detection of late-mRNA of HCMV by NASBA technique is rapid, sensitive and specific detection for HCMV active infection. The detected result correlates with clinical symptoms. It can monitor HCMV infection of allo-PBSCT transplanted recipients and provide indication to antiviral therapy.

Adolescent↗

PubMed1998

Genetic immunization generates cellular and humoral immune responses against the nonstructural proteins of the hepatitis C virus in a murine model.

Exposure to hepatitis C virus (HCV) is associated with a high prevalence of persistent viral infection and the development of chronic liver disease and hepatocellular carcinoma. Recovery from acute infection may depend upon the generation of broad-based cellular immune responses to viral structural and nonstructural proteins. We used the DNA-based immunization approach in BALB/c mice to determine whether the HCV nonstructural proteins NS3, NS4, and NS5 will induce Ab responses, CD4+ Th cell proliferation, and cytokine release in response to stimulation by recombinant proteins as well as generate CD8+ CTL activity both in vitro and in vivo. We found that the nonstructural proteins were particularly good immunogens and produced cellular immune responses when administered as a DNA construct. Indeed, a tumor model was established following inoculation of syngenic SP2/0 cells stably transfected with NS5. We observed protection against tumor formation and growth only in mice immunized with the NS5-encoding DNA construct, establishing the generation of significant CTL activity in vivo by this technique. The results indicate that genetic immunization may define the cellular immune response of the host to HCV nonstructural proteins and is a promising approach for vaccine development.

Animals↗

PubMed1995

A rabbitpox virus serpin gene controls host range by inhibiting apoptosis in restrictive cells.

Poxviruses are unique among viruses in encoding members of the serine proteinase inhibitor (serpin) superfamily. Orthopoxviruses contain three serpins, designated SPI-1, SPI-2, and SPI-3. SPI-1 encodes a 40-kDa protein that is required for the replication of rabbitpox virus (RPV) in PK-15 or A549 cells in culture (A. N. Ali, P. C. Turner, M. A. Brooks, and R. W. Moyer, Virology 202:305-314, 1994). Examination of nonpermissive human A549 cells infected with an RPV mutant disrupted in the SPI-1 gene (RPV delta SPI-1) suggests there are no gross defects in protein or DNA synthesis. The proteolytic processing of late viral structural proteins, a feature of orthopoxvirus infections associated with the maturation of virus particles, also appears relatively normal. However, very few mature virus particles of any kind are produced compared with the level found in infections with wild-type RPV. Morphological examination of RPV delta SPI-1-infected A549 cells, together with an observed fragmentation of cellular DNA, suggests that the host range defect is associated with the onset of apoptosis. Apoptosis is seen only in RPV delta SPI-1 infection of nonpermissive (A549 or PK-15) cells and is absent in all wild-type RPV infections and RPV delta SPI-2 mutant infections examined to date. Although the SPI-1 gene is expressed early, before DNA replication, the triggering apoptotic event occurs late in the infection, as RPV delta SPI-1-infected A549 cells do not undergo apoptosis when infections are carried out in the presence of cytosine arabinoside. While the SPI-2 (crmA) gene, when transfected into cells, has been shown to inhibit apoptosis, our experiments provide the first indication that a poxvirus serpin protein can inhibit apoptosis during a poxvirus infection.

Animals↗

PubMed1987

Spectrum of natural antibodies against five HTLV-III antigens in infected individuals: correlation of antibody prevalence with clinical status.

The genome of the HTLV-III/LAV retrovirus, the etiologic agent of the acquired immunodeficiency syndrome (AIDS), encodes the viral structural proteins (envelope and core proteins), the reverse transcriptase, a transactivation protein (tat-III), as well as two other proteins (3'orf, sor) of unknown function. We studied the prevalence of natural antibodies against envelope, gag, 3'orf, sor, and tat-III in the sera of HTLV-III infected individuals in an attempt to correlate clinical status with seropositivity to specific HTLV-III antigens. We selected 101 sera; 16 were obtained from normal donors with no known risk factors, and 85 were from patients with full-fledged AIDS (28 cases), AIDS-related complex (ARC, 22 cases), and healthy people at risk (homosexuals, intravenous [IV] drug users, relatives of AIDS patients; 35 cases). Seropositivity for antibodies against the envelope (gp41) and gag antigens (p15, p24) was determined by Western blot using disrupted HTLV-III virions. Of the 101 sera, all 16 from nonrisk donors and 3/35 from healthy at-risk donors were negative for antibodies against either the gp41 or p15 and p24. The remaining 82 sera were seropositive for either the gp41 and/or the p15 and p24. All sera were then tested against the three known HTLV-III antigens (3'orf, sor, and tat-III) that have been synthesized in bacteria. Our data indicate that all the HTLV-III antigens tested are immunogenic in vivo. No significant difference in antibody prevalence to gp41 (close to 100%) and to the 3'orf, sor, and tat-III proteins (approximately 50%) was observed with regard to stage of the disease. In contrast, the prevalence of antibodies against the core antigens decreased from approximately 100% in infected people with no clinical signs of disease to 50% in ARC and AIDS patients. The percentage of patients seropositive for all five antigens tested was increased in the AIDS group. These results indicate that the greatest antibody prevalence was obtained using viral envelope antigen and further suggest that screening with the newly identified 3'orf, sor, and tat-III proteins as antigens would confer no further diagnostic advantage. The pattern of natural antibodies observed during disease progression did not suggest any pathogenetic mechanism.

AIDS-Related Complex↗

PubMed2006

Rescue of infectious rift valley fever virus entirely from cDNA, analysis of virus lacking the NSs gene, and expression of a foreign gene.

Rift Valley fever virus (RVFV) (genus Phlebovirus, family Bunyaviridae) has a tripartite negative-strand genome, causes a mosquito-borne disease that is endemic in sub-Saharan African countries and that also causes large epidemics among humans and livestock. Furthermore, it is a bioterrorist threat and poses a risk for introduction to other areas. In spite of its danger, neither veterinary nor human vaccines are available. We established a T7 RNA polymerase-driven reverse genetics system to rescue infectious clones of RVFV MP-12 strain entirely from cDNA, the first for any phlebovirus. Expression of viral structural proteins from the protein expression plasmids was not required for virus rescue, whereas NSs protein expression abolished virus rescue. Mutants of MP-12 partially or completely lacking the NSs open reading frame were viable. These NSs deletion mutants replicated efficiently in Vero and 293 cells, but not in MRC-5 cells. In the latter cell line, accumulation of beta interferon mRNA occurred after infection by these NSs deletion mutants, but not after infection by MP-12. The NSs deletion mutants formed larger plaques than MP-12 did in Vero E6 cells and failed to shut off host protein synthesis in Vero cells. An MP-12 mutant carrying a luciferase gene in place of the NSs gene replicated as efficiently as MP-12 did, produced enzymatically active luciferase during replication, and stably retained the luciferase gene after 10 virus passages, representing the first demonstration of foreign gene expression in any bunyavirus. This reverse genetics system can be used to study the molecular virology of RVFV, assess current vaccine candidates, produce new vaccines, and incorporate marker genes into animal vaccines.

Animals↗

PubMed1983

U.V. enhanced reactivation of U.V.-and gamma-irradiated adenovirus in normal human fibroblasts.

An enhanced reactivation (UVER) of U.V.-irradiated as well as of gamma-irradiated human adenovirus type 2 (Ad 2) was detected following infection of normal human fibroblasts which had been pre-irradiated with U.V. light. U.V.-irradiated or non-irradiated fibroblasts were infected with either non-irradiated or irradiated Ad 2, and at 48 hours after infection cells were examined for the presence of viral structural antigens (Vag) using immunofluorescent staining. Results obtained using 5 different normal fibroblast strains showed that irradiation of host monolayers with 10J/m2 immediately prior to infection gave a U.V. enhanced reactivation (UVER) factor +/- standard error equal to 3 . 1 +/- 1 . 2 for virus U.V.-irradiated with 1 . 2 x 10(3) J/m2, and 2 . 1 +/- 0 . 5 for virus gamma-irradiated with 2 x 10(4) Gy. For a fixed survival of about 5 . 9 x 10(-2) for irradiated virus, the efficiency of UVER for gamma-irradiated virus was about 0 . 18, slightly less than the value of about 0 . 24 obtained for U.V.-irradiated virus. The results of time course experiments indicated that while U.V.-irradiation of normal host monolayers prior to infection gave rise to an increased rate of Vag formation for infection by unirradiated Ad 2, U.V.-irradiation of the cells increased the proportion of cells able to repair U.V.-damaged virus as well as allowing an earlier onset and/or increased rate of synthesis of Vag from a U.V.-damaged template. Similar experiments involving gamma-ray enhanced reactivation (gamma-RER) of irradiated Ad 2 indicated that gamma-RER and UVER may operate, in part at least, by different mechanisms in normal human cells.

Adenoviruses, Human↗

PubMed1990

Prevalence of antibodies to the core protein P17, a serological marker during HIV-1 infection.

Studies on monitoring the immune response to viral structural proteins during human immunodeficiency virus (HIV-1) infection have established the significance of antibodies to the core protein p24 during the progression of the disease. We have studied the prevalence of antibodies to the core protein p17 in order to study their diagnostic and prognostic significance in the pathogenesis of HIV-1. Full-length HIV-1 p17, molecularly cloned and expressed in Escherichia coli was purified by immunoaffinity chromatography using an HIV-1 p17-specific monoclonal antibody. A highly sensitive enzyme-linked immunoassay was developed using the purified recombinant p17 as the serological target to detect antibodies to p17. The results indicated that antibodies to p17 decline during progression of disease, with the decline being more dramatic as patients moved from asymptomatic to AIDS-related complex (ARC). Patient specimens deficient in p24 antibody, but having detectable levels of antibody to p17 were almost always positive for p24 antigen. Under these conditions, p17 antibody is an important serological marker because it provides a more consistent marker for core antigens during HIV-1 infection.

Acquired Immunodeficiency Syndrome↗