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Journal of Virology, May 2000, p. 4698-4704, Vol. 74, No. 10
Division of Human Biology, Fred Hutchinson
Cancer Research Center, Seattle, Washington
981091; Department of Pathology,
Colorado State University, Fort Collins, Colorado
805232; and Department of Pathology,
University of Washington, Seattle, Washington
981953
Received 16 November 1999/Accepted 16 February 2000
Jaagsiekte sheep retrovirus (JSRV) is a type D retrovirus
associated with a contagious lung tumor of sheep, ovine pulmonary carcinoma. Other than sheep, JSRV is known to infect goats, but there
is no evidence of human infection. Until now it has not been possible
to study the host range for JSRV because of the inability to grow this
virus in culture. Here we show that the JSRV envelope protein (Env) can
be used to pseudotype Moloney murine leukemia virus (MoMLV)-based
retrovirus vectors and that such vectors can transduce human cells in
culture. We constructed hybrid retrovirus packaging cells that express
the JSRV Env and the MoMLV Gag-Pol proteins and can produce
JSRV-pseudotype vectors at titers of up to 106 alkaline
phosphatase-positive focus-forming units/ml. Using this high-titer
virus, we have studied the host range for JSRV, which includes sheep,
human, monkey, bovine, dog, and rabbit cells but not mouse, rat, or
hamster cells. Considering the inability of the JSRV-pseudotype vector
to transduce hamster cells, we used the hamster cell line-based
Stanford G3 panel of whole human genome radiation hybrids to
phenotypically map the JSRV receptor (JVR) gene
within the p21.3 region of human chromosome 3. JVR is likely a new
retrovirus receptor, as none of the previously identified retrovirus
receptors localizes to the same position. Several chemokine receptors
that have been shown to serve as coreceptors for lentivirus infection
are clustered in the same region of chromosome 3; however, careful
examination shows that the JSRV receptor does not colocalize with any
of these genes.
Jaagsiekte sheep retrovirus (JSRV)
is the causative agent of a contagious lung cancer of sheep known as
ovine pulmonary carcinoma (OPC), also known as sheep pulmonary
adenomatosis or jaagsiekte. OPC is a veterinary problem with
significant economic impact in several countries. In addition, OPC
shares characteristics with human bronchioalveolar carcinoma (BAC)
(12, 32, 49), and BAC represents about 25% of human lung
cancer cases (6). Lung cancer being the most common fatal
form of cancer in humans (10), recent interest in JSRV stems
from the hypothesis that OPC could be useful as a naturally occurring
animal model for understanding the mechanism of pulmonary
carcinogenesis (26, 49).
JSRV has been classified as a type D retrovirus, based on genomic
organization, but has a type B-like Env protein (61). The
sheep genome carries multiple copies of JSRV-like endogenous sheep
retrovirus (ESRV) sequences (25, 27, 61), but subsequent studies have shown that JSRV is an exogenous virus distinct from ESRV
sequences (4, 5, 44) and is specifically associated with
OPC. Recent studies by Palmarini et al. (48) using an
infectious molecular clone of JSRV have confirmed that JSRV is the
causative agent of OPC. The mechanism of oncogenesis by JSRV is not
known. JSRV has the genomic organization of a simple
replication-competent retrovirus with no known oncogenes. The
incubation period in naturally acquired OPC seems to range from months
to years, suggesting insertional mutagenesis. However, OPC can be
induced experimentally in 3 to 4 weeks, suggesting a mechanism of
action more similar to that of a transforming retrovirus.
The main sites of JSRV replication and assembly are the transformed
epithelial cells of the lung, especially the alveolar type II cells
(45). The lung fluid and tumor extracts of infected sheep
can be used for virus isolation and also for experimentally transmitting the disease to lambs by intratracheal inoculation (14, 37, 59), suggesting that the virus is stable in lung fluid. The stability of the virus in lung fluid as well as the ability
to infect the epithelial cells of the lung indicate that JSRV vectors
may be useful for gene transfer into the lung for human diseases such
as cystic fibrosis. Even if the vectors were unable to transduce human
airway epithelial cells, characterization of this virus would provide
insights into developing improved vectors for transduction of the lung.
To study JSRV as a prospective retroviral vector, we first wanted to
test whether the JSRV Env protein could be used to pseudotype a
commonly used Moloney murine leukemia virus (MoMLV)-based retrovirus vector. Once this was established by transient transfection and the
JSRV Env was shown to promote entry into human cells, we generated a
packaging cell line for producing high-titer JSRV-pseudotype retrovirus
vector which allowed us to investigate the host range for JSRV Env.
Study of the JSRV host range has been hindered so far by the lack of an
in vitro culture system for growing the virus, and only recently has an
infectious molecular clone of the virus been developed (48).
Subsequently, we used a human-hamster whole genome radiation hybrid
(RH) panel to precisely localize the JSRV receptor (JVR) within human
chromosome 3p21.3.
Cell culture.
Mammalian cells, including SSF-123 primary
sheep skin fibroblasts (gift from William Osborne, University of
Washington, Seattle), HT-1080 human fibrosarcoma cells (American Type
Culture Collection [ATCC] cell line CCL-121), 293 human kidney
epithelial cells (ATCC CRL 1573), IB3 immortalized human bronchial
epithelial cells (62), HeLa cervical carcinoma cells (ATCC
CCL-2), NIH 3T3 thymidine kinase-deficient mouse embryo fibroblasts
(60), Mus dunni tail fibroblasts (11),
D17 canine osteosarcoma cells (ATCC CRL-6248), 208F rat embryo
fibroblasts (51), MDBK bovine kidney epithelial cells (ATCC
CCL-22), Vero African green monkey kidney epithelial cells (ATCC
CCL-81), MF-NAN primary mouse (BALB/c) fibroblasts, MF-H1 primary mouse
(C57BL/6) fibroblasts, and RbTE rabbit tracheal epithelial cells (gifts
from Christine Halbert, Fred Hutchinson Cancer Research Center), were
grown in Dulbecco's modified Eagle's medium supplemented with 10%
fetal bovine serum (Hyclone). RbTE cells were immortalized by
transduction with the human papillomavirus E6 and E7 genes in a
retrovirus vector, LXSN16E6E7 (24). G355 feline embryonic
brain cells (15) were grown in McCoy's medium supplemented
with 15% fetal bovine serum. CHO cells (ATCC CCL-61), A23 hamster
cells, and the A23-derived RH clones (57) (gifts from Davis
Cox, Stanford University) were grown in minimal essential medium-alpha
supplemented with 10% fetal bovine serum.
Retroviral vectors and virus titer.
The nomenclature for
retroviral vectors and pseudotypes has been discussed before
(41). LAPSN is an MoMLV-based vector encoding the human
placental alkaline phosphatase (AP) and the neomycin phosphotransferase
proteins (42). Vectors with a JSRV pseudotype were made by
using the pSX2.Jenv plasmid (Fig. 1),
which was constructed by inserting the 1,883-bp
MslI-Ecl136 fragment of JSRV-JS7
containing the Env coding region into the BsaAI- and
MscI-cut 4,239-bp backbone of the pSX2 plasmid
(38) by blunt-end ligation. JSRV-JS7 is a
proviral clone derived from a
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Retrovirus Vectors Bearing Jaagsiekte Sheep
Retrovirus Env Transduce Human Cells by Using a New Receptor
Localized to Chromosome 3p21.3
ABSTRACT
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
INTRODUCTION
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
MATERIALS AND METHODS
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
phage library of genomic DNA from the
JS7 cell line that was derived from a spontaneous case of OPC
(unpublished results). Retrovirus vector titers were determined as
described previously, by assaying for either AP+
focus-forming units (FFU) (17) or G418-resistant
colony-forming units (CFU) (40).
View larger version (10K):
[in a new window]
FIG. 1.
JSRV Env expression plasmid pSX2.Jenv. Abbreviations:
SV40 pA, the early-region polyadenylation signal from simian virus 40;
LTR, retrovirus long terminal repeat; SD and SA, splice donor and
acceptor sites, respectively. The ATG start and TAA stop codons of Env
are shown.
Generation of JSRV-pseudotype retrovirus packaging cells.
Stable retrovirus packaging cells expressing the JSRV Env were made
using the techniques described previously for the construction of 10A1
murine leukemia virus (MLV)-pseudotype packaging cell lines
(38). Briefly, NIH 3T3 cells that express the MoMLV Gag-Pol proteins (LGPS cells [39]) were cotransfected with
plasmid pSX2.Jenv and a plasmid encoding hygromycin phosphotransferase
(pSV2
13-hyg; gift from Paul Berg, Stanford University) at a 20:1 or
100:1 ratio, and 24 hygromycin-resistant clones were isolated. These
clonal cell lines were tested for their ability to produce retrovirus vectors by measuring the titer of vector produced by the cells after
the cells were transduced with the LAPSN vector made by using PT67
packaging cells (38). HT-1080 human cells were used as
targets for measurement of the vector titer. The clonal line that
produced the highest-titer vector was clone PJ14.
Marker rescue assay. SSF and HT-1080 cells were plated at 105 cells per 6-cm dish on day 1, transduced with LAPSN(PT67) virus at a multiplicity of infection of ~1 in the presence of Polybrene (4 µg/ml) on day 2, and trypsinized and replated in G418 (active concentration of 250 µg/ml for SSF and 400 µg/ml for HT-1080 cells). These polyclonal populations of cells carrying the LAPSN vector were used in the marker rescue assay for helper virus as described before (38). Briefly, SSF/LAPSN or HT-1080/LAPSN cells were plated at 5 × 105 cells per 6-cm dish on day 1, infected with 0.5 ml of LAPSN(PJ) test virus (6 × 105 AP FFU/ml) per dish in the presence of Polybrene on day 2, and trypsinized and split 1:10 every 2 to 3 days for 2 weeks while being kept at high density to facilitate potential virus spread. After 2 weeks, medium harvested from confluent dishes of cells was tested for LAPSN vector rescue and transfer using SSF cells as targets. MoMLV was used as a positive control to show that helper virus could rescue the LAPSN vector in these cells. The passaged SSF/LAPSN and HT-1080/LAPSN cells were also stained for AP to ensure that they retained the LAPSN vector.
RH mapping of JVR and STRL33 genes. The Stanford G3 panel of human whole-genome hybrid cell lines was used for phenotypic RH mapping (www-shgc.stanford.edu/Mapping/rh/) (57). For mapping JVR, the RH cell lines were plated at 5 × 104 cells per well in a 6-well plate and exposed to LAPSN(JSRV) vector the next day. AP assays were performed as explained above, and AP+ FFU were counted to measure transduction.
To map the STRL33 gene, we used the Stanford G3 panel RH DNA (Research Genetics, Huntsville, Ala.) for genotypic mapping. PCR was performed with the STRL33-specific primers 5'-GCCAGGGTTTCGAGAAGCTGCTCTGGAATT-3' and 5'-TCATAGTCCCTGGTGCTAGTTATTCTGGAT-3'. Genomic DNA samples from the A3 hamster cell line (57) and the RM human lymphoblastoid cell line (57) were used as negative and positive controls, respectively. All PCR amplifications were performed with an initial denaturation step at 94°C for 2 min, followed by 35 cycles of amplification at 94°C for 30 s, at 62°C for 1 min, and 68°C for 4 min, with a final extension at 68°C for 10 min. The PCR products were electrophoresed on 1% agarose gels and visualized by ethidium bromide staining.| |
RESULTS |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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JSRV Env protein can pseudotype an MoMLV-based retrovirus vector
and promote transduction of human cells.
We tested whether the
JSRV Env could be incorporated into virions containing MoMLV Gag-Pol
proteins and an MoMLV-based vector by transient transfection of the
JSRV Env expression plasmid pSX2.Jenv (Fig. 1) into LGPS/LAPSN cells.
These cells contain the MoMLV-based LAPSN vector and the pLGPS plasmid
for expression of MoMLV Gag-Pol proteins (38). Transfection
of the pSX2 plasmid DNA expressing the 10A1 MLV Env (38) was
used as a positive control. Two days after transfection, the medium
from these cells was harvested and assayed for vector production using
SSF-123 sheep skin fibroblasts and HT-1080 human fibrosarcoma cells as
targets for transduction (Table 1). Both
cell types could be transduced by the JSRV-pseudotype LAPSN vector,
showing the ability of JSRV Env to pseudotype MoMLV-based vectors
packaged with MoMLV Gag proteins as well as the ability of JSRV Env to
promote entry into human cells. The JSRV-pseudotype vector titer was
~10-fold higher on the sheep than on the human cells. In
contrast, the titers of the 10A1- and xenotropic-pseudotype LAPSN
vectors were at least 10-fold higher on the human than on the sheep
cells, showing the preference of the JSRV-pseudotype vector for sheep
cells. These results indicated the potential to develop a
JSRV-pseudotype packaging line capable of producing high-titer virus
capable of transducing human cells.
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High-titer vector production in the absence of replication-competent virus. Stable JSRV-pseudotype retrovirus packaging lines expressing JSRV Env and MoMLV Gag-Pol proteins were generated, and individual clones were screened for packaging function as described in Materials and Methods. Of 24 clones tested for LAPSN vector production after introduction of the vector into the clonal cell lines, 6 could produce the vector at a titer of >103 AP+ FFU/ml, 10 did not produce any vector (<10 AP+ FFU/ml), and the rest produced intermediate titers. To show that these JSRV-pseudotype packaging cells could be used to generate stable vector-producing cell lines, the clone which was able to produce the highest titer virus (PJ14) was plated at 105 cells per 6-cm dish on day 1, transduced at a multiplicity of infection of ~1 with LAPSN(PT67) virus in the presence of Polybrene on day 2, and trypsinized and replated at a 1:100 or 1:500 dilution in medium containing G418 (500 µg/ml, active) on day 3. Individual clones were selected and screened for LAPSN vector titer using SSF cells as targets. Titers as high as 6 × 105 AP+ FFU/ml were obtained, demonstrating that the JSRV-pseudotype packaging cells can be used to generate high-titer retrovirus vectors. Testing of the LAPSN vector produced from a high-titer clone by a marker rescue assay showed that the preparations were free of replication-competent virus (<1 FFU/ml).
Host range of JSRV Env.
The JSRV-pseudotype LAPSN vector was
used to measure the ability of JSRV Env to promote transduction of a
variety of mammalian cells (Table 2). The
JSRV-pseudotype vector transduced various human cells but at titers
~10-fold lower than that obtained with SSF-123 cells. Although the
JSRV-pseudotype vector transduced various human cell lines, including
IB3 bronchial epithelial cells, HT-1080 fibrosarcoma cells, and 293 kidney epithelial cells, it could only transduce HeLa human cervical
carcinoma cells at low levels. In addition to sheep and human cells,
the vector transduced a wide range of mammalian cells, including
monkey, bovine, dog, and rabbit cells. The vector also transduced G-355
cat cells but at very low levels. The vector was unable to transduce
wild or laboratory mouse cells, rat cells, or hamster cells. All cell types that exhibited low to undetectable transduction by the
JSRV-pseudotype vector (
20 infectious units per ml) could be
transduced with a 10A1 MLV-pseudotype LAPSN vector made by using PT67
retrovirus packaging cells (38) at titers of
>103 G418-resistant CFU/ml (HeLa cells) or AP+
FFU/ml (all other cell types) (data not shown), indicating that the
LAPSN vector and MoMLV Gag-Pol proteins are functional in these cells,
as expected, and that the block to infection was at the level of virus
entry mediated by the JSRV Env.
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JVR maps to region p21.3 of human chromosome 3 at a site different from those of other retrovirus receptors. JSRV-pseudotype vectors transduce human but not hamster cells, indicating that it might be possible to map the position of the JSRV receptor by analyzing the susceptibility of human-hamster RH cell lines to transduction by a JSRV vector. We used the G3 panel of human RH cell lines from the Stanford Human Genome Center (SHGC) (57) for phenotypic mapping of JVR. The transduction result for the 83 ordered hybrid cell lines was 00000000000000000000000000000000001100001000000R000000000000001000100000000R0R00001, where 0 indicates no transduction (<10 FFU/ml), 1 indicates transduction (>100 FFU/ml), and R indicates an indeterminate result (cell clone not available for analysis). This result was submitted to the SHGC RH Server v4.0 (www-shgc.stanford.edu/RH/index.html), which mapped JVR at a distance of 18 cR10,000 (centiray distance for RH cells made using 10,000 rads of irradiation) from marker SHGC-11855 on chromosome 3 with a highly significant LOD score (log10 of the likelihood ratio) of 6.77. Subsequently, we used the multiple integrated maps at the National Center for Biotechnology Information (NCBI) Entrez Genomes site (www.ncbi.nlm.nih.gov/Entrez/Genome/org.html) to map JVR to a position within region p21.3 of chromosome 3.
The chromosomal locations of most other known retrovirus receptors have been determined (Table 3). Many of these map to chromosomes other than chromosome 3, showing that JSRV does not use these receptors for cell entry. Careful examination of the p21.3 region of human chromosome 3 showed that none of the previously mapped retroviral receptors localize to the same position. However, the lentivirus receptor STRL33 (also called Bonzo and TYMSTR) had been assigned to chromosome 3 but had not been more precisely localized (34). These studies indicated that JVR is probably a new retroviral receptor but might be the same as STRL33.
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STRL33 (Bonzo) maps to 3p21.3 region, ~500 kb telomeric to the
285-kb CCR cluster.
To determine whether or not STRL33 might
function as the JSRV receptor, we used the Stanford G3 panel RH DNA for
mapping the STRL33 gene, as explained in Materials and Methods. The PCR
results for DNA samples from the 83 ordered hybrids was
000000000000 0100R00100000000000000010000110000000000000000000001 010010000R001000010,
where 0 indicates PCR negative, 1 indicates PCR positive, and R
indicates an indeterminate result. This bar code was submitted to the
SHGC RH Server v4.0, which mapped STRL33 at a distance of 13 cR10,000 (LOD, 9.46) from marker SHGC-12886. Using the
multiple integrated maps at the NCBI Entrez Genomes site, we have
localized the STRL33 gene to about 500 kb away from the CCR cluster in
chromosome 3p21.3 and about 7.5 Mb from JVR, thus showing that STRL33
and JVR do not localize to the same position and JVR is not likely to
be any of the known retroviral receptors (Fig.
2).
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DISCUSSION |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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JSRV has recently gained prominence mainly because of the similarity of OPC to BAC in humans, suggesting that OPC can be used as an animal model to understand the process of pulmonary carcinogenesis. However, studies on JSRV have been hindered so far by the lack of a cell culture system for propagating the virus. Recently, a full-length infectious proviral molecular clone of JSRV was isolated from a natural case of OPC, and a cell culture system was developed to propagate the virus by replacing the upstream U3 with the cytomegalovirus early promoter (48). JSRV has been known to infect sheep and goats, but there is no evidence of human infection. Our studies show that the JSRV Env can be used to pseudotype MoMLV-based retroviral vectors containing MoMLV Gag-Pol proteins, thus providing a means for studying the host range of the viral Env protein. We have been able to generate packaging cell lines based on JSRV Env and MoMLV Gag-Pol proteins that can produce JSRV-pseudotype retroviral vectors at titers of up to 106 AP+ FFU/ml. Our results show that the JSRV Env promotes entry into sheep, human, monkey, bovine, dog, and rabbit cells but not mouse (laboratory or wild), rat, or hamster cells. The inability of the vector to transduce mouse or rat cells is unfortunate, as it prevents us from using rodents for studying JSRV pathogenesis or in vivo gene transfer to the lung. Poor transduction of HeLa cells suggests that the JSRV receptor (JVR) may not be constitutively expressed in all cell types.
This is the first report showing the ability of JSRV Env to transduce human cells and suggesting the feasibility of developing JSRV as a prospective retroviral vector for gene transfer to the lung. Although both viral (18, 53) and nonviral (2, 31) methods have been extensively studied, efficient gene transfer to the airway epithelial cells has proved difficult (21, 22, 50). Previous studies in our laboratory have shown that amphotropic retroviral vectors can efficiently transduce the basal and secretory airway epithelial cells in vitro, but in vivo delivery resulted in no detectable transduction in the intact normal airway epithelium and a low transduction rate in the wounded epithelium (23). This low retroviral transduction in vivo is due to the low abundance of retroviral receptors and inhibition of amphotropic retroviral vector transduction by pulmonary surfactant (63) or by soluble chondroitin sulfates in pleural effusions (7). Although JSRV infects several cell types in vivo (30, 45, 47, 48), the epithelial tumor cells in the lungs of sheep have been shown to be the major sites of viral replication (45), suggesting a natural tropism of the virus for the airway epithelial cells. Furthermore, OPC can be experimentally reproduced in newborn lambs by intratracheal inoculation of concentrated lung fluid or tumor extracts collected from OPC-affected sheep (14, 37, 59), demonstrating the stability of the virus in lung fluid. We are currently studying the ability of JSRV to infect airway epithelial cells and its stability in the presence of pulmonary surfactant.
The ability of JSRV Env to promote infection of human cells in culture could be relevant to the epidemiology of human lung cancer, especially with regard to nonsmokers exposed to sheep in which OPC is endemic. Although there is no proof for JSRV involvement in human lung carcinoma, the possibility of viral etiology cannot be excluded because of the similarity of BAC to OPC and the multifocal and multiclonal nature of some BAC cases (46). Several factors could explain the absence of evidence for human infection with JSRV, such as lack of immunological reagents to detect human infections. There has been no report of any serological study to evaluate human sera for JSRV antibodies. Alternatively, the JSRV Env might be able to bind to receptors and mediate entry of the viral genome, but some of the viral replicative elements may not be functional in human cells, resulting in postentry or replication blocks. It is known that the JSRV Gag-Pol proteins are functional during viral assembly in human cells, as evidenced by the use of an infectious molecular clone of JSRV to produce the virus in 293 human epithelial cells (48). However, their functionality during reverse transcription and integration of viral DNA in human cells is unknown. Another important factor might be the presence of transcriptionally active ESRV sequences in the sheep genome, which may induce tolerance to JSRV antigens in sheep and allow the virus to propagate and establish an infection. On the contrary, humans and other animals may develop a strong immune response leading to virus clearance.
Chromosome localization provides an important alternative approach to interference analysis to determine retroviral receptor usage. The advantages of chromosome localization are that extensive cross-interference analyses between the test virus and the growing number of existing viruses need not be performed, and the technique is informative for viruses that do not exhibit strong interference to infection by viruses that use the same receptor. Utilizing the inability of JSRV Env to promote infection of hamster cells, we have used a panel of human-hamster whole-genome RH cell lines to localize the JSRV receptor (JVR) gene to the p21.3 region of human chromosome 3. Although the majority of known retroviral receptors do not localize to chromosome 3, most of the CC-chemokine receptor genes (CCRs) which have been identified as coreceptors for lentiviruses have been shown to map within the 3p21.3 region (55). Careful analysis of the mapping data revealed that JVR does not map to the same positions as most of these receptors, being ~7 Mb away from the 285-kb cluster of CCR3, -1, -2, -5, and -6 and farther away from CCR4, CCR8, and CCR10 (Fig. 2). The lentivirus receptor CX3CR1 has recently been mapped to the 3p24 region (35), leaving one other lentivirus receptor, STRL33 (Bonzo), in question (34). Using the G3 panel of RH DNA, we have localized the STRL33 gene 500 kb telomeric to the CCR cluster in region 3p21.3 and about 7.5 Mb away from JVR. These results indicate that JVR is a new retroviral receptor in human cells.
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ACKNOWLEDGMENTS |
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We thank Jeanette Bishop for the isolation, cloning, and sequencing of the JSRV-JS7 provirus; Christine Halbert for providing the RbTE primary rabbit tracheal epithelial cells, MF-NAN primary mouse (BALB/c) fibroblasts, and MF-H1 primary mouse (C57BL/6) fibroblasts; William Osborne for providing the sheep skin fibroblasts; and David Cox for providing the RH cell lines.
This work was supported by grants DK47754 (A.D.M.), HL54881 (A.D.M.), and CA59116 (J.C.D.) from the National Institutes of Health. S.K.R. was supported by institutional funding.
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FOOTNOTES |
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* Corresponding author. Mailing address: Fred Hutchinson Cancer Research Center, Room C2-023, 1100 Fairview Ave. N., Seattle, WA 98109-1024. Phone: (206) 667-2890. Fax: (206) 667-6523. E-mail: dmiller{at}fhcrc.org.
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
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Journal of Virology, May 2000, p. 4698-4704, Vol. 74, No. 10
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