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PubMed2000

Mouse mammary tumor virus-like ENV gene sequences in human breast tumors and in a lymphoma of a breast cancer patient.

DNA sequences with very high similarity (95-98%) to the mouse mammary tumor virus (MMTV) ENV gene have been amplified by PCR in 38.5% of human breast tumors and in <2% of normal breast tissue (Wang et al., Cancer Res., 55: 5173-5179, 1995). Intrigued by these findings, which suggested an exogenous viral etiology for a certain percentage of human breast tumors, we have screened a panel of human breast tumors and normal breast tissue for the presence of MMTV-like DNA sequences. Using similar PCR procedures and stringent hybridization techniques, we have detected the presence of MMTV-like ENV gene sequences in 37% of the human breast tumors that we have analyzed. DNA sequencing has shown these sequences to be 99% homologous to the BR6 strain of MMTV and 100% homologous to the GR and C3H strains of MMTV. We have not detected these MMTV-like sequences in normal breast tissue. However, we have detected these sequences by PCR and stringent hybridization in a T-cell lymphoma of a breast cancer patient who was simultaneously diagnosed with both diseases. Our results support the possibility of an exogenous retroviral etiology for a certain percentage of human breast tumors. Our results also suggest that a similar exogenous retroviral etiology may exist for certain human T-cell lymphomas. In many inbred strains of mice, both breast cancer and T-cell lymphoma are caused by MMTV, hence, in a certain percentage of humans, one or both of these diseases may be caused by an MMTV-like retroviral entity.

Adult↗
PubMed1995

Immunization trial of cats with a replication-defective adenovirus type 5 expressing the ENV gene of feline immunodeficiency virus.

Our aim was to develop a recombinant replication-defective adenovirus suitable for the vaccination of cats against feline immunodeficiency virus. We first demonstrated that this vector was able to transfer a marker gene (E. coli beta-galactosidase) in feline cells in vitro. We then constructed an adenovirus type 5 expressing the Feline Immunodeficiency Virus (FIV) envelope (ENV) gene of the Wo isolate in the absence of the rev gene (Ad-ENV-Wo). Ad-ENV-Wo was then tested in four cats in a 3 injections scheme (at day 0, day 30 and day 210). Four other control cats received Ad-gp50, a similar recombinant adenovirus expressing gp50 (Ad-gp50) of pseudorabies virus (PRV). Viruses were formulated in two different kind of oil adjuvants (water/oil and water/oil/water), a protocol previously shown to enhance the immune response against the virus-induced protein. The control cats developed neutralizing antibodies against PRV, demonstrating the potency of recombinant human adenovirus 5 (Ad5) as a vector in cats. Antibody responses appeared after the first injection and were higher with the water/oil/water formulation than with the water/oil controls. However, none of the four cats vaccinated with Ad-ENV-Wo developed antibodies against two peptides of the envelope protein. Animals were challenged with 20 infectious doses 50% of the strain Wo. All of them developed antibodies against FIV within 4 to 5 weeks, and FIV virus could be isolated from all.

Adenoviridae↗
PubMed1996

The mouse mammary tumor virus env gene is the source of a CD8+ T-cell-stimulating peptide presented by a major histocompatibility complex class I molecule in a murine thymoma.

CD8+ cytotoxic T cells recognize their targets by the presence of unique peptide bound to a major histocompatibility complex (MHC) class I molecules on the cell surface. The MHC molecules normally display thousands of distinct peptides, making it difficult to identify individual antigenic peptides, their protein precursors, and their relative importance in the T-cell response. Here we used the EL-4 tumor-specific lacZ-inducible KZ30.6 T cell as a probe for detecting the peptide/MHC ligand that was generated in cells transfected with an EL-4 cDNA library. These expression screens allowed identification of a mouse mammary tumor virus (MMTV) transcript as the source of the antigenic peptide presented by the Kb MHC molecule. The antigenic activity was encoded within the MMTV env gene and was defined by the octapeptide ANYDFICV (AFV8). Synthetic AFV8 stimulated KZ30.6 T cells at picomolar concentrations and coeluted with one of two active peptides in HPLC-fractionated extracts of EL-4 cells. The AFV8/Kb complex was also recognized by two other EL-4-specific T cells. The results illustrate a novel strategy for identifying T-cell-stimulating antigens and suggest that the MMTV env gene and its naturally processed AFV8 peptide product can serve as a model for study of antigen processing and tumor immunotherapy.

Amino Acid Sequence↗
PubMed1995

HPRS-103 (exogenous avian leukosis virus, subgroup J) has an env gene related to those of endogenous elements EAV-0 and E51 and an E element found previously only in sarcoma viruses.

The avian leukosis and sarcoma virus (ALSV) group comprises eight subgroups based on envelope properties. HPRS-103, an exogenous retrovirus recently isolated from meat-type chicken lines, is similar to the viruses of these subgroups in group antigen but differs from them in envelope properties and has been assigned to a new subgroup, J. HPRS-103 has a wide host range in birds, and unlike other nontransforming ALSVs which cause late-onset B-cell lymphomas, HPRS-103 causes late-onset myelocytomas. Analysis of the sequence of an infectious clone of the complete proviral genome indicates that HPRS-103 is a multiple recombinant of at least five ALSV sequences and one EAV (endogenous avian retroviral) sequence. The HPRS-103 env is most closely related to the env gene of the defective EAV-E51 but divergent from those of other ALSV subgroups. Probing of restriction digests of line 0 chicken genomic DNA has identified a novel group of endogenous sequences (EAV-HP) homologous to that of the HPRS-103 env gene but different from sequences homologous to EAV and E51. Unlike other replication-competent nontransforming ALSVs, HPRS-103 has an E element in its 3' noncoding region, as found in many transforming ALSVs. A deletion found in the HPRS-103 U3 EFII enhancer factor-binding site is also found in all replication-defective transforming ALSVs (including MC29, which causes rapid-onset myelocytomas).

Alpharetrovirus↗
PubMed1992

An O-linked carbohydrate neutralization epitope of HIV-1 gp 120 is expressed by HIV-1 env gene recombinant vaccinia virus.

Previous studies have disagreed about the presence of O-linked carbohydrate epitopes on gp 120 of HIV, although antibodies against short-chain O-linked glycans neutralize HIV infection and block syncytium formation in vitro. To settle this question, we analysed the O-linked glycans of gp 120 by chemical methods using purified HIV-1 gp 120 from cells infected with recombinant vaccinia virus solely expressing gp 160 or gp 120. Alkaline borohydride degradation of recombinant gp 120 released monosaccharides and also slightly larger structures (di/trisaccharides) by a beta-elimination, confirming the presence of simple O-linked oligosaccharides. The functional activity as neutralisation epitopes of the O-linked oligosaccharides expressed on recombinant gp 120 was preserved, since fusion between uninfected CD4+ cells and cells infected with recombinant vaccinia was blocked by monoclonal antibodies to the O-linked oligosaccharides of gp 120. Although the mechanism for HIV induction of O-linked oligosaccharide neoantigens is unknown, these results indicate that the O-linked neutralization epitopes are inherent to the glycoprotein itself, and that the unusual appearance of simple O-linked oligosaccharides on gp 120 is independent of any interaction between the host cell and retroviral genes other than env.

Animals↗
PubMed1998

Expression of mouse mammary tumor virus-like env gene sequences in human breast cancer.

We have reported previously (Wang et al, Cancer Res., 55: 5173-5179, 1995) the presence of a 660-bp sequence that is 90-98% homologous to the env gene of mouse mammary tumor virus in 38% of 314 unselected breast cancer samples, in some breast cancer cell lines, and in 1.8% of the 107 normal breast specimens from reduction mammoplasties. In this communication, we have investigated whether the 660-bp sequence or a smaller 256-bp sequence within the 660 bp were expressed in breast tumors, normal breasts, and breast cancer cell lines by means of reverse transcription-PCR. The results indicated that expression of the 660-bp sequence was detected in 66% of the sequence-positive breast tumors studied and in none of the negative tumors or normal breasts and that the 256-bp sequence was expressed in all of the env-positive breast cancer cell lines tested. Sequence analysis revealed that the expressed 660-bp sequence is 98% homologous to the env gene of mouse mammary tumor virus with only one small stretch of 46 bp homologous to endogenous viral sequences. The presence and expression of this sequence is related to a group of human breast cancers in which the concept of a retroviral etiology can be entertained.

Animals↗
PubMed1998

Genetic heterogeneity of env gene of feline immunodeficiency virus obtained from multiple districts in Japan.

Feline immunodeficiency virus (FIV) infection is widespread in many countries. FIV isolates have been classified into five distinct subtypes, A, B, C, D and E based on their env gene sequences. Several reports indicate that most of the FIVs isolated in Japan belong to subtype B which includes the first Japanese isolate, TM2 strain. To examine the distribution of FIV subtypes in Japan, proviral DNA sequences of the env gene were directly amplified by nested PCR from FIV-infected cats that had been kept in multiple districts throughout Japan. Phylogenetic analysis of the 11 strains showed that four FIV subtypes, A, B, C and D, were present in Japan. Among these subtypes, subtypes B and D were the two most common subtypes in Japan, and they were mainly distributed in the eastern and western parts of Japan, respectively. The present study provides information that is fundamental for development of a vaccine to protect against FIV infection in cats.

Amino Acid Sequence↗
PubMed1993

Stable expression of the transfected HIV-1 env gene in a human B cell line: characterization of gp120-expressing clones and immunobiological studies.

The env gene of human immunodeficiency virus type 1 (HIV-1) encodes gp 120/41 which plays an important role in the viral infection process and pathogenesis. The surface glycoprotein gp120 is a candidate molecule for the development of a subunit vaccine against HIV-1-induced acquired immunodeficiency syndrome (AIDS). However, thorough studies on the immunobiology of this molecule are hampered by the lack of a suitable model. With this background in mind, and in order to learn more on anti-gp120 cellular immunity, we attempted to develop gp120-expressing human cell clones. Thus by transfecting a human lymphoid cell line of B lineage (Raji), which is known to be resistant to the natural killer cell activity, with an expression vector encoding the envelope and vpu, we established three clones that stably express gp120/41 and vpu. The surface glycoprotein gp 120 is also expressed on the cell surface of these clones. The transfected cells from syncytia with CD4+ human cell lines as well as with peripheral blood mononuclear cells (PBMC) leading to the death of the fused cells. This observation represents additional evidence for the eventual depletion of CD4+ viral targets that fuse with adjacent HIV-infected, gp 120-expressing cells. The latent Epstein-Barr virus genome present in the transfected cells, was not induced to express the lytic cycle antigens. The densities of the surface expression of a number of molecules examined remained unchanged in the transfected cells except for the surface IgM, which increased significantly (P < 0.05) in two clones. One of the clones exhibited a significantly (P < 0.05) reduced proliferation rate as compared to the other clones. The transfected cells of all the three clones showed a significantly (P < 0.01) increased susceptibility to lysis by the PBMC from normal, healthy individuals in a 16-hr 51Cr-release assay. This is the first report of the MHC- and antibody-independent lysis of human cells transfected with the HIV-1 surface glycoprotein. The transfected cells also served as targets in a gp120-specific antibody-dependent cellular cytotoxicity assay. We anticipate that the present model will prove very useful for studying the gp120-specific immune responses in HIV-infected individuals.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Interruption of env gene expression depending on the length of the SV40 early region used for the polyA signal.

In order to invent a screening system to check in vivo gene function and the efficiency of gene transfer mediated by a retroviral vector system, we established a novel packaging cell, PacNIH/A8, based on the neuropathogenic retrovirus A8-V. To construct the expression vector, pA8(Psi-), which expresses the genes gag, pol and env derived from A8-V, the SV40 early region was used for the polyadenylation signal (polyA signal). When a 0.85 kbp fragment in the SV40 early region was employed for the expression vector (pA8(Psi-)beta), env expression was abolished. This abolition was rescued by shortening the SV40 early region to 0.14 kbp (pA8(Psi-)delta). The NHI3T3 cells transfected with pA8(Psi-)delta showed expressions of both env and gag genes.

Animals↗
PubMed1991

Genetic analysis of the Rous sarcoma virus subgroup D env gene: mammal tropism correlates with temperature sensitivity of gp85.

Subgroup D avian sarcoma and leukosis viruses can penetrate a variety of mammalian cells in addition to cells from their natural host, chickens. Sequences derived from the gp85-coding domain within the env gene of a mammal-tropic subgroup D virus (Schmidt-Ruppin D strain of Rous sarcoma virus [SR-D RSV]) and a non-mammal-tropic subgroup B virus (Rous-associated virus type 2) were recombined to map genetic determinants that allow penetration of mammalian cells. The following conclusions were based on host range analysis of the recombinant viruses. (i) The determinants of gp85 that result in the mammal tropism phenotype of SR-D RSV are encoded within the 160 codons that lie 3' of codon 121 from the corresponding amino terminus of the gp85 protein. (ii) Small linear domains of the SR-D RSV gp85-coding domain placed in the subgroup B background did not yield viruses with titers equal to that of the subgroup D virus in a human cell line. (iii) Recombinant viruses that contained subgroup D sequences within the hr1 variable domain of gp85 showed modest-to-significant increases in infectivity on human cells relative to chicken cells. A recombinant virus that contained three fortuitous amino acid substitutions in the gp85-coding domain was found to penetrate the human cell line and give a titer similar to that of the subgroup D virus. In addition, we found that the subgroup D virus, the mutant virus, and recombinant viruses with an increased mammal tropism phenotype were unstable at 42 degrees C. These results suggest that the mammal tropism of the SR-D strain is not related to altered receptor specificity but rather to an unstable and fusogenic viral glycoprotein. A temperature sensitivity phenotype for infectivity of mammalian cells was also observed for another mammal-tropic avian retrovirus, the Bratislava 77 strain of RSV, a subgroup C virus, but was not seen for any other avian retrovirus tested, strengthening the correlation between mammal tropism and temperature sensitivity.

Animals↗
PubMed1980

env Gene of Rous sarcoma virus: identification of the gene product by cell-free translation.

Cell-free translation of polyadenylic acid-selected, denatured virion 70S RNA of the Schmidt-Ruppin strain of Rous sarcoma virus (subgroup A) yields a 64,000-Mr polypeptide which is specifically immunoprecipitated by a group-specific serum raised against envelope glycoprotein gp85. This polypeptide is not synthesized from the virion RNA of the replication-defective mutant rdNY8SR-A, which contains an extensive deletion within the envelope (env) gene. From this genetic evidence we conclude that the 64,000-Mr polypeptide represents the nonglycosylated product of the env gene and propose the designation of P64env. The 64,000-Mr polypeptide is translated from a 26S to 28S polyadenylated RNA species, whereas the p60src product is synthesized from a 20S to 22S RNA, and both Pr76gag and P180gag-pol are synthesized predominately from 34S RNA. The product of the env gene of Rous-associated virus-2 was also identified by cell-free translation.

Avian Leukosis Virus↗
PubMed1992

An activation-dependent, T-lymphocyte-specific transcriptional activator in the mouse mammary tumor virus env gene.

Transcription of the complete mouse mammary tumor virus (MMTV) proviral genome in mouse cells is controlled by a strong promoter in its long terminal repeat. In the mouse T lymphoma EL4, there is a second, activation-dependent transcriptional initiation site within the envelope (env) gene, from which a short mRNA is generated, encoding the open reading frame of the long terminal repeat. We now report the isolation of a segment of the MMTV env gene (called META, for MMTV env transcriptional activator) which has the expected transcription-activating properties seen in EL4.E1 cells. Namely, it induces activation-dependent, T-lymphocyte-specific transcription of a chloramphenicol acetyltransferase reporter gene. It is active in mouse or human T-helper lymphocyte lines when they are stimulated to transcribe lymphokine genes but is inactive in unstimulated T-helper cells, fibroblasts, a cytotoxic T-lymphocyte line, and a mastocytoma cell line. Its activity is inhibited by cyclosporin A, a specific inhibitor of lymphokine transcription. Several forms of the META have been isolated from EL4.E1 cells, a mouse T-helper cell hybridoma, and from BALB/c spleen cells. Linked to the heterologous thymidine kinase promoter, a 400-bp portion of it is an inducible, orientation-independent, and cyclosporin A-sensitive transcriptional activator in T-helper cells.

Animals↗
PubMed2004

Analysis of full-length HIV type 1 env genes indicates differences between the virus infecting T cells and dendritic cells in peripheral blood of infected patients.

Dendritic cells (DC) are targets for HIV-1 infection and may harbor distinct populations of virus variants. To test this hypothesis full length env genes have been amplified and sequenced from DC and T cells purified from the blood of five symptomatic HIV-1-infected patients. For three of the patients, showing slow and slow/standard disease progression, distinct subsets of HIV variants infected DC and T cells, and the diversity of the DC-derived env genes was less than that observed in T cells. Amino acid substitutions differentiating DC and T cell variants were dispersed throughout the length of the glycoproteins and were patient/HIV-1 strain specific. However, the V1 and V2 domains of T cell-derived clones were generally shorter than those from DC. These findings suggest that there may be distinct populations of HIV-1 variants infecting blood DC and T cells in patients showing slow and slow/standard disease progression.

Adult↗
PubMed2006

Use of a novel assay based on intact recombinant viruses expressing green (EGFP) or red (DsRed2) fluorescent proteins to examine the contribution of pol and env genes to overall HIV-1 replicative fitness.

Multiple studies have described a reduction in the replicative fitness of HIV-1 isolates harboring mutations that confer resistance to antiretroviral drugs. Contradictory results, however, have been obtained depending on the methodology used in each study (Quinones-Mateu, M.E., Arts, E.J., 2002. Fitness of drug resistant HIV-I: methodology and clinical implications. Drug Resist. Update 5, 224-233), affecting our understanding of the potential relationship of viral replicative fitness with HIV-1 disease. It has been demonstrated previously that both pol and env genes play a major role in HIV-1 replicative fitness of clinical isolates. Therefore, measuring clinically relevant replicative fitness using recombinant viruses where a single mutation and/or viral gene have been introduced does not seem like a reasonable approach in this era of multi-target antiretroviral therapy. A novel method was developed to measure HIV-1 replicative fitness based on recombinant viruses expressing the enhanced green fluorescent (EGFP) or the Discosoma sp. red fluorescent (DsRed2) proteins in a HIV-1NL4-3 backbone. Contrary to previous designs to analyze HIV-1 fitness, these replication competent viruses were created in an intact viral genetic background (without deleting or affecting the expression of any viral gene). This new system was used to evaluate the contribution of drug-resistance mutations in the pol and env genes to overall viral replicative fitness (in the presence and absence of drug pressure) using direct growth competition experiments. Mutations in pol showed a stronger effect on HIV-1 replicative fitness than mutations in the env gene associated with resistance to enfuvirtide, corroborating the plasticity of the later gene to accept mutations and the sensibility of the protease and reverse transcriptase enzymes to drug-associated primary mutations. In conclusion, a new protocol was used to measure HIV-1 replicative fitness in either the presence or absence of antiretroviral drugs, which may be used as a high-throughput assay to help us understand the clinical significance of viral fitness.

Cell Line↗
PubMed2005

Evidence for heterogeneous selective pressures in the evolution of the env gene in different human immunodeficiency virus type 1 subtypes.

Recent studies have demonstrated the emergence of human immunodeficiency virus type 1 (HIV-1) subtypes with various levels of fitness. Using heterogeneous maximum-likelihood models of adaptive evolution implemented in the PAML software package, with env sequences representing each HIV-1 group M subtype, we examined the various intersubtype selective pressures operating across the env gene. We found heterogeneity of evolutionary mechanisms between the different subtypes with a category of amino acid sites observed that had undergone positive selection for subtypes C, F1, and G, while these sites had undergone purifying selection in all other subtypes. Also, amino acid sites within subtypes A and K that had undergone purifying selection were observed, while these sites had undergone positive selection in all other subtypes. The presence of such sites indicates heterogeneity of selective pressures within HIV-1 group M subtype evolution that may account for the various levels of fitness of the subtypes.

Amino Acid Sequence↗
PubMed1991

Individual-specific patterns of human variable genomic regions detected by a DNA probe from the HIV-1 env gene.

It was postulated that similar genetic elements that are 'hot spots' for genetic variation might exist in both the HIV-1 and the human genome. To test this possibility a short repeated sequence from a region of variability in the HIV-1 glycoprotein (env) gene was amplified and used as a probe for blot hybridization with human genome DNA. Human genomic regions were hybridized and characterized by a set of polymorphic restriction DNA fragments. The pattern of the restriction fragments was individual specific. Thus a DNA probe from the HIV-1 env gene can serve as a genetic marker for hybridization with human genome regions and for the identification of individuals.

Amino Acid Sequence↗
PubMed1993

Loss of antigenic epitopes as the result of env gene recombination in retrovirus-induced leukemia in immunocompetent mice.

The murine leukemia virus, E-55+ virus, induces a thymic lymphoma/leukemia in 100% of BALB.K mice infected as adults after a latent period of 4 months or more (Pozsgay et al., Virology 173, 330-334, 1989). Two molecular clones of virus designated E-55+ and E-55- based on their ability to encode the E-55 epitope detected by the monoclonal antibody 55 (mAb 55) were isolated from a leukemic BALB.K mouse inoculated with a biologically cloned E-55+ virus (Chesebro et al., Virology 112, 131-144, 1981). Env gene sequence analysis of E-55+ and E-55- clones showed that the E-55- virus was generated from the E-55+ virus as the result of a recombination between E-55+ virus and the endogenous ecotropic virus, emv-1, carried in the genome of the BALB.K mouse strain. The recombinant E-55- virus is replication competent. This recombination event and the consequential expression of E-55- virus consistently occur in immunocompetent BALB.K mice inoculated with the E-55+ virus and appear to play a role in the loss of epitopes recognized by virus neutralizing antibodies. The loss of these epitopes apparently allows the virus to evade the host immune response.

Animals↗
PubMedDate not supplied

[The family of env genes of avian retroviruses: molecular analysis of Rous sarcoma virus adapted to duck cells].

For the elucidation of the molecular basis of RSV adaptation to conditionally permissive host from the genome library of duck embryo fibroblasts, transformed by Rous sarcoma virus in 30 passages on these cells, recombinant bacteriophages that include provirus sequences, were obtained. Complete and transformation-defective proviruses were characterized, nucleotide sequences of their env-genes were compared with their counterparts the original RSV (Pr-RSV-C) and with viruses of other subgroups (A, B, D and E). The possible relation of the revealed changes in domains coding gp85 and gp37, with the changes of chicken RSV characteristics during adaptation to duck cells is discussed.

Animals↗