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Previous Article | Next Article 
Journal of Virology, July 2000, p. 6193-6197, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Resistance to Friend Murine Leukemia Virus Infection Conferred by
the Fv-4 Gene Is Recessive but Appears Dominant from the
Effect of the Immune System
Fengmin
Zhang,1,2
Lamin Ta
Ya,1
Yasumasa
Iwatani,1
Kyoko
Higo,1
Yasunori
Suzuki,1
Masakazu
Tanaka,1
Tomomi
Nakahara,1
Takeshi
Ono,1
Hiroyuki
Sakai,1
Kagemasa
Kuribayashi,3 and
Akinori
Ishimoto1,*
Laboratory of Gene Analysis, Department of
Viral Oncology, Institute for Virus Research, Kyoto University,
Sakyo-ku, Kyoto 606-8507,1 and
Department of Bioregulation, School of Medicine, Mie
University, Tsu, Mie 514-8507,3 Japan, and
Department of Microbiology, Harbin Medical University, Harbin
150086, People's Republic of China2
Received 4 February 2000/Accepted 29 March 2000
 |
ABSTRACT |
Fv-4 is a mouse gene that dominantly confers resistance
to infection with Friend murine leukemia virus (F-MuLV) (S. Suzuki, Jpn. J. Exp. Med. 45:473-478, 1975). However, the resistance caused by
Fv-4 is recessive in nude mice, which suggests that
immunological effects play important roles in this resistance in vivo
(K. Higo, Y. Kubo, Y. Iwatani, T. Ono, M. Maeda, H. Hiai, T. Masuda, K. Kuribayashi, F. Zhang, T. Lamin, A. Adachi, and A. Ishimoto, J. Virol. 71:750-754, 1997). To determine the immunological effect on the
resistance in vivo, we infected immunologically immature newborn mice
homozygous (Fv-4r/r) and heterozygous
(Fv-4r/
) for Fv-4. Although the
Fv-4r/r mice showed complete resistance to
F-MuLV whether infected neonatally or as adolescents, the
Fv-4r/ mice showed high sensitivity to viral
proliferation and disease induction when infected as newborns but
complete resistance when infected as adolescent mice. To confirm the
immunological effect on the resistance in adolescent mice with the
Fv-4r/r and Fv-4r/
genotypes, we examined the effect of an immunosuppressant drug, FK506,
on the resistance. The mice with the Fv-4r/r
genotype treated with FK506 still showed resistance, but the mice with
the Fv-4r/ genotype became highly sensitive
to F-MuLV infection. Flow cytometric analysis to detect the
Fv-4 gene product showed that the Fv-4 gene
product was expressed on the cells from newborn and adolescent mice.
The Fv-4 gene product was also detected on the cells from the FK506-treated mice as well as on those from untreated mice. However, a quantitative difference in the gene product between the
cells with the Fv-4r/r and
Fv-4r/ genotypes was detected by indirect
staining for flow cytometry. These results show that the resistance to
F-MuLV infection conferred by the Fv-4 gene is originally
recessive, but it looks dominant in adolescent mice mainly because of
the effect of the immune system.
| |
TEXT |
Susceptibility to retroviral
infection is influenced by the genetic background of the host (2,
3, 4). Among many genes influencing Friend murine leukemia virus
(F-MuLV) infection (5), Fv-1, Fv-2,
and Fv-4 have been extensively studied. Fv-4 was
molecularly cloned much earlier than the others (1, 18, 19, 20,
26). However, much about the Fv-4 gene is poorly understood. Fv-4 is located on chromosome 12, and resistance
to exogenous infection with ecotropic MuLV is reported to be inherited as a simple Mendelian dominant gene (12, 25, 31). We
previously reported that transplantation of bone marrow cells from
BALB/Fv-4 mice, i.e., Fv-4 congenic BALB/c mice
(Fv-4r/r) established by breeding wild-type mice
carrying the Fv-4 resistance gene with susceptible
(Fv-4/) BALB/c mice (done by Odaka et al.
[25]), can prevent the development of murine AIDS in
susceptible mice infected with the murine AIDS virus (22).
The resistant mice were found to have a glycoprotein equivalent to the
exogenous ecotropic MuLV envelope on their lymphocytes, while mice with
the Fv-4/ genotype did not (10, 11, 14,
32), and sequence analysis characterized the Fv-4 gene
as a truncated MuLV sequence containing the 3' portion of the
pol region, the entire env gene, and the 3' long
terminal repeat (9, 13), so that viral interference by
competitive blocking of the virus receptor became a prime candidate for
the Fv-4 restriction mechanism. However, there is no direct evidence that the Fv-4 gene product binds directly to the
receptor. Despite the complete expression of Fv-4 resistance
in vivo described above, cells carrying the Fv-4 gene are
partially permissive to virus infection in vitro (22, 30,
31), and some reports have suggested a more complex mechanism of
Fv-4-mediated resistance in vivo (7).
Studies on the susceptibility of nude mice to MuLV infection suggested
that immunological effects play important roles in the resistance to
F-MuLV infection caused by Fv-4 in nude mice (7,
16). To better understand the role of the immune system in the
resistance, we investigated the gene dosage effect of the Fv-4 gene product under immune-deficient conditions. In this
study, two inbred strains of mice with the Fv-4 resistance
gene, FRG and BALB/Fv-4 mice, were used. The FRG mouse,
formerly called the G mouse and supplied by Chugai Pharmaceutical Co.
Ltd., is the first laboratory strain shown to be resistant to F-MuLV by virtue of carrying the Fv-4 gene (28, 29).
Newborn (younger-than-24-h-old) and adolescent (4-week-old) BALB/c,
BALB/Fv-4, FRG, (BALB/c × BALB/Fv-4)F1, and (BALB/c × FRG)F1 mice were infected with 0.1 and 0.5 ml,
respectively, of NB-tropic F-MuLV (about 5.2 log focus-forming units
[FFU]/0.2 ml by the UV-XC test [27] on SC-1 cells
[6]) intraperitoneally to compare the susceptibilities
of mice with immature and mature immune systems to F-MuLV infection
(Table 1). Among the adolescent mice,
only the BALB/c mice without Fv-4 that were inoculated with the virus developed the disease and were susceptible to viral proliferation. No proliferation of virus was detected 10 or 25 days
after inoculation in the mice with the Fv-4r/r
genotype or the Fv-4r/ genotype when they were
inoculated as adolescents. However, (BALB/c × BALB/Fv-4)F1 and (BALB/c × FRG)F1 mice with the Fv-4r/
genotype developed the disease within 10 days when inoculated neonatally. Viral proliferation was also detected in the spleens of the
mice with Fv-4r/ genotype 10 days after
inoculation. Many mice with the Fv-4/ and
Fv-4r/ genotypes inoculated neonatally started
to die at around 2 weeks after infection. It was thus confirmed that
the F-MuLV resistance phenotype of BALB/Fv-4 and FRG mice
appeared to be inherited as a dominant trait when the mice were
infected as adolescents but as a recessive trait when they were
infected neonatally.
To determine whether the Fv-4 gene was expressed in newborn
as well as in adolescent mice, cells from thymus and spleen were stained directly with fluorescein isothiocyanate (FITC)-conjugated anti-Fv-4 immunoglobulin G (IgG) and indirectly with
anti-Fv-4 mouse serum and FITC-conjugated goat anti-mouse
IgG for flow cytometry analysis. The anti-Fv-4 IgG was
purified from the sera of BALB/c mice
(Fv-4/) immunized with spleen cells from
BALB/Fv-4 mice (Fv-4r/r) by using a
protein A-Sepharose column and labeled with FITC, and FITC-conjugated
anti-Fv-4 IgG was prepared. FITC-conjugated goat anti-mouse
IgG was purchased from MBL Co. Ltd. (Nagoya, Japan).
As shown in Fig. 1, the specificity of
the anti-Fv-4 antibody was confirmed by staining of thymic
cells from adult BALB/c, (BALB/c × BALB/Fv-4)F1, and BALB/Fv-4 mice,
because it was blocked by anti-Fv-4 serum but not by normal
BALB/c serum in direct staining. Blocking with anti-Fv-4
BALB/c serum (Fig. 1C) showed an increased size of the negative peak in
heterozygous (BALB/c × BALB/Fv-4)F1 and
homozygous BALB/Fv-4 mice accompanied by loss of population with at least greater than 1 log unit staining intensity compared with
blocking with normal serum (Fig. 1B). The expression of the Fv-4 gene was clearly detected on thymic cells from newborn
BALB/Fv-4 and (BALB/c × BALB/Fv-4)F1 mice by both direct and indirect
methods (Fig. 2) (10).
Although only the expression of Fv-4 on thymus cells is
shown in this paper, fluorescence-activated cell sorter analysis of the
fluorescence detected on spleen cells was shown in our previous paper
(7). The level of fluorescence detected on the spleen cells
was almost the same as that detected on the thymic cells, except for
the staining of B cells among spleen cells by FITC-conjugated
anti-mouse IgG goat serum (data not shown). However, the indirect
staining, which may be low in specificity but high in sensitivity, was
interesting. By the indirect staining, some difference between the
Fv-4r/r and Fv-4r/
genotypes in the intensity of fluorescence showing Fv-4 gene expression was observed on cells from both adolescent (Fig. 1) and
newborn (Fig. 2) mice.
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FIG. 1.
Fv-4 expression on thymic cells from
4-week-old BALB/c, (BALB/c × BALB/Fv-4)F1,
and BALB/Fv-4 mice detected by flow cytometry with direct (A
to C) and indirect (D and E) staining. After the Fc receptor was
blocked with rat anti-mouse CD16-CD32 monoclonal antibody, cells were
treated with FITC-conjugated anti-Fv-4 antibody (A). As a
blocking test, cells were blocked with serum from normal BALB/c mice
(B) or with anti-Fv-4 BALB/c serum (C) and were stained with
FITC-conjugated anti-Fv-4 antibody. For indirect staining,
cells were first treated with normal BALB/c serum (D) or
anti-Fv-4 BALB/c serum (E) and were then stained with
FITC-conjugated goat anti-mouse IgG antibody.
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FIG. 2.
Fv-4 expression on thymic cells from newborn
BALB/c, (BALB/c × BALB/Fv-4)F1, and
BALB/Fv-4 mice detected by flow cytometry with direct (A)
and indirect (B) staining.
|
|
To confirm the immunological effects on the susceptibility of mice with
the Fv-4 gene to F-MuLV infection, we examined the susceptibility of mice treated with the immune-suppressant drug FK506.
FK506, an antibiotic isolated from the fermentation broth of
Streptomyces tukubaenis and reported to be a potent
immunosuppressant (8, 15, 21), was supplied by Fujisawa
Pharmaceutical Co. Ltd. The 4-week-old mice were treated with FK506 at
5.0 mg/kg/day subcutaneously every other day. The mice were infected
with 0.5 ml of F-MuLV intraperitoneally on the day after the third
administration of FK506. From the next day of virus infection, mice
continued to be treated with FK506 every other day for an additional 7 and 12 times. After infection for 16 and 26 days, mice were killed to
examine the effects of the immunosuppressant on resistance to viral
replication and disease development (Table
2). Although there were no prominent
effects of FK506 on the susceptibility of BALB/c
(Fv-4/) and BALB/Fv-4
(Fv-4r/r) mice to F-MuLV infection, (BALB/c × BALB/Fv-4)F1
(Fv-4r/) mice were rendered susceptible to
F-MuLV infection by the treatment. Viral proliferation in the spleen
was detected in all FK506-treated mice with the
Fv-4r/ genotype, even when splenomegaly was
not detected. The reason why the spleen weights for the FK506-treated
virus-infected (BALB/c × BALB/Fv-4)F1
(Fv-4r/) mice are not equivalent to those for
virus-infected BALB/c (Fv-4/) mice may
depend on the effect of heterozygously coded Fv-4 gene expression. As a prominent side effect of FK506 treatment, growth disorders, such as loss of body weight or interruption of increase of
body weight, including spleen weight, was often observed in both
infected and uninfected mice. The effect of FK506 on Fv-4 gene expression in cells from thymuses and spleens of FK506-treated mice was analyzed by flow cytometry (Fig.
3). Expression of Fv-4 was
detected on the cells from the mice with the
Fv-4r/ genotype treated with FK506 every other
day for a total of 3 or 10 times, as well as on the cells from
untreated mice (Fig. 3). The data obtained by flow cytometry suggested
that conversion from resistance to sensitivity does not depend on the
decrease of Fv-4 gene expression but depends on other
factors, such as suppression of the immune reaction by FK506.
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TABLE 2.
Effect of the immunosuppressant drug FK506 on the
susceptibility of mice with the Fv-4 gene to
F-MuLV infection
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FIG. 3.
Fv-4 expression on thymic cells from
FK506-treated mice detected by flow cytometry with direct (A) and
indirect (B) staining. The thymic cells were prepared from the mice
treated with FK506 every other day for a total of 10 times.
|
|
Newborn mice are more sensitive than adolescent mice to MuLV in general
(5, 16). Although it has been known for F-MuLV infection to
develop into erythoroid leukemia even in mice infected as adolescents
(7), the adolescent (BALB/c × BALB/Fv-4)F1 mice were resistant to F-MuLV
infection. That flow cytometry for Fv-4 gene expression did
not detect clear differences between the cells from adolescent and
newborn mice suggests that the immunological immaturity of newborn
F1 mice is an important factor in their susceptibility to
F-MuLV infection.
It has been reported that the Fv-1 locus has two codominant
alleles, Fv-1n and Fv-1b.
Cells carrying the Fv-1n allele are susceptible
to N-tropic MuLVs, whereas cells carrying the
Fv-1b allele are susceptible to B-tropic viruses
(17, 23). The Fv-2 locus encodes a dominant host
factor that confers susceptibility to F-MuLV-induced erythroleukemia
(18, 24). Our observations about the susceptibilities of
newborn mice and mice treated with the immunosuppressant FK506 to
F-MuLV infection suggest that Fv-4 is essentially a
recessive gene that looks dominant because it acts in cooperation with
other factors. The difference in susceptibility between the homozygous
(Fv-4r/r) and heterozygous
(Fv-4r/) mice under immune-deficient
conditions may depend on a quantitative difference in the
Fv-4 gene product due to the gene dosage effect detected by
indirect staining.
Homozygotes (Fv-4r/r) showed complete resistance
even under the immune-deficient conditions in vivo, but tissue culture
cells from these mice are susceptible to viral infection in vitro. This discrepancy in susceptibility to F-MuLV in vivo and in vitro suggests the presence of other mechanisms influencing resistance conferred by
Fv-4 in vivo in addition to immune response.
| |
ACKNOWLEDGMENTS |
Fengmin Zhang and Lamin Ta Ya contributed equally to this work.
We thank Toshio Hattori and Hiroshi Hiai for useful technical advice.
We also thank Yuki Sato, Chiemi Tajima, Masako Saka, and Yumi Inukai
for animal care.
This work was partly supported by Grants-in-Aid for Science Research
and Cancer Research from the Ministry of Education, Science and Culture
of Japan and by Grants-in-Aid for AIDS research from the Ministry of
Health and Welfare of Japan to Akinori Ishimoto and Hiroyuki Sakai.
| |
FOOTNOTES |
*
Corresponding author. Mailing address: Laboratory of
Gene Analysis, Institute for Virus Research, Kyoto University,
Sakyo-ku, Kyoto 606-8507, Japan. Phone: 81-75-751-4039. Fax:
81-75-751-3995. E-mail:
aishimot{at}virus.kyoto-u.ac.jp.
| |
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Journal of Virology, July 2000, p. 6193-6197, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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