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PubMed1994

Keratinocytes immortalized by human papillomavirus-18 exhibit alterations dependent upon host genetic background and complexity of viral genes transfected.

Keratinocytes immortalized by the human papillomaviruses (HPVs) vary in cell morphology, growth properties, resistance to inducers of terminal differentiation, and karyotype. To determine the contribution of the host cell genetic background and the HPV genes to these cellular alterations, we have generated and characterized 6 human keratinocyte lines from two different newborn foreskins (A and B) using either the full-length HPV18 genome or the isolated HPV18 E6/E7 genes. The growth properties of the immortalized lines were found to correlate with the complexity of HPV genes present in the transfected vector. Interestingly, cell lines established from foreskin A revealed common chromosomal alterations regardless of the HPV construct utilized for immortalization, and these karyotypic changes differed from those observed in cell lines established from foreskin B, which exhibited their own characteristic aneuploid profile. Thus, chromosomal alterations of HPV-immortalized cells are in part determined by the host genetic background.

Cell Line↗
PubMed2002

Effect of genetic background and diet on plasma fibrinogen in mice. Possible relation with susceptibility to atherosclerosis.

Many epidemiological studies suggest that elevated plasma fibrinogen concentrations form one of the most important independent risk factors in blood for cardiovascular disease and particularly atherosclerosis in humans. To clarify the effect of genetic factors, diets and their interactions on plasma fibrinogen concentrations, we examined plasma fibrinogen levels in four strains of mice, which differ in their susceptibility to cholesterol-induced atherosclerosis. When maintained on basal diet, two strains 129/J and C3H/HeJ exhibited a significantly higher plasma fibrinogen concentration (2.1 and 1.9 mg/ml) than C57BL/6J and BALB/C strains (1.5 and 1.4 mg/ml). The strongest and most rapid (1 week) increase of plasma fibrinogen (by all semi-synthetic diets) is observed in C57BL/6J mice, which are known to be highly susceptible to diet-induced atherosclerosis. After a period of 8 weeks an increase in plasma fibrinogen of approximately 30-50% was observed in all strains on all semi-synthetic diets. Remarkably, no increase was observed in the fibrinogen Aalpha- Bbeta- and gamma-chain mRNA levels in the liver on the same diets. These mRNA levels were even decreased by approximately 20-50% in all strains on an extremely atherogenic diet. It was found that: genetic background determines the plasma fibrinogen levels on basal diet; plasma fibrinogen levels are altered by diet; the extent of these changes depends on the genetic background: surprisingly, this increase of fibrinogen in plasma is independent of transcription; the diet-induced increase of fibrinogen was very fast in the very highly atherosclerosis-susceptible strain C57BL/6J having a low basal fibrinogen level, and very slow in the atherosclerosis-resistant strain C3H/HeJ having a high basal fibrinogen level. It might be concluded that it is the kinetics of the response of fibrinogen to diet rather than the actual level, which relates to atherosclerosis susceptibility.

Alpha-Globulins↗
PubMed2006

Genetic background determines response to hemostasis and thrombosis.

BACKGROUND: Thrombosis is the fatal and disabling consequence of cardiovascular diseases, the leading cause of mortality and morbidity in Western countries. Two inbred mouse strains, C57BL/6J and A/J, have marked differences in susceptibility to obesity, atherosclerosis, and vessel remodeling. However, it is unclear how these diverse genetic backgrounds influence pathways known to regulate thrombosis and hemostasis. The objective of this study was to evaluate thrombosis and hemostasis in these two inbred strains and determine the phenotypic response of A/J chromosomes in the C57BL/6J background. METHODS: A/J and C57Bl/6J mice were evaluated for differences in thrombosis and hemostasis. A thrombus was induced in the carotid artery by application of the exposed carotid to ferric chloride and blood flow measured until the vessel occluded. Bleeding and rebleeding times, as surrogate markers for thrombosis and hemostasis, were determined after clipping the tail and placing in warm saline. Twenty-one chromosome substitution strains, A/J chromosomes in a C57BL/6J background, were screened for response to the tail bleeding assay. RESULTS: Thrombus occlusion time was markedly decreased in the A/J mice compared to C57BL/6J mice. Tail bleeding time was similar in the two strains, but rebleeding time was markedly increased in the A/J mice compared to C57BL/6J mice. Coagulation times and tail morphology were similar, but tail collagen content was higher in A/J than C57BL/6J mice. Three chromosome substitution strains, B6-Chr5A/J, B6-Chr11A/J, and B6-Chr17A/J, were identified with increased rebleeding time, a phenotype similar to A/J mice. Mice heterosomic for chromosomes 5 or 17 had rebleeding times similar to C57BL/6J mice, but when these two chromosome substitution strains, B6-Chr5A/J and B6-Chr17A/J, were crossed, the A/J phenotype was restored in these doubly heterosomic progeny. CONCLUSION: These results indicate that susceptibility to arterial thrombosis and haemostasis is remarkably different in C57BL/and A/J mice. Three A/J chromosome substitution strains were identified that expressed a phenotype similar to A/J for rebleeding, the C57Bl/6J background could modify the A/J phenotype, and the combination of two A/J QTL could restore the phenotype. The diverse genetic backgrounds and differences in response to vascular injury induced thrombosis and the tail bleeding assay, suggest the potential for identifying novel genetic determinants of thrombotic risk.

Journal Article↗
PubMed1991

Influence of the genetic background and carrier protein on the antibody response to GnRH.

A vaccine against the gonadotropin releasing hormone (GnRH) is being developed as an immunological method for the treatment of prostatic enlargement. The work described here was aimed at investigating the influence of the genetic background on immune responses to GnRH conjugated to diphtheria toxoid (DT). Mice of different strains were injected with the conjugate and the antibody levels against GnRH and DT quantitated in order to examine the effect of genetic background on immune responses to the hapten and the carrier. All immunized animals produced antibodies to DT. Anti-GnRH antibodies were generated by all strains of mice except 129. The low anti-GnRH response in the 129 strain mice did not appear to be MHC-linked, as C57BL/6 mice, which bear the same MHC haplotype as 129 mice, were able to generate a strong anti-GnRH response. The non-responsiveness to the hapten (GnRH) in 129 strain mice was overcome by the use of an 'alternate carrier' approach.

Animals↗
PubMed1983

Hypomyelinated mutant mice. V. Relationship between jp and jpmsd re-examined on identical genetic backgrounds.

jp and jpmsd, two allelic mutations in the mouse that sharply reduce the amount of CNS myelin, produce diseases that can be distinguished morphologically only by their severity. This has raised the question of whether the two mutations are truly distinguishable. Since the two mutations have never been maintained on the same genetic background, correct quantitative and morphological comparison have not been possible. We have prepared a B6C3H stock of jp on the same genetic background as the available stock of jpmsd. In this jp stock, behavioral abnormalities, relative proportion of myelinated axons, and major morphological characteristics of the disease in situ are unchanged from the previous jp stock. The jp disease continues to be more severe than that of jpmsd. However, tissue from the new B6C3H stock myelinates better in organotypic culture than previous jp stocks. The increase in myelination is advantageous, not only for accurate comparison of the two alleles but for all culture studies of jp. Strictly comparable strains or stocks should be utilized in any comparative studies of closely related mutations such as jp and jpmsd.

Alleles↗
PubMed2002

Familial abdominal aortic aneurysm: a systematic review of a genetic background.

BACKGROUND: Familial clustering of the abdominal aortic aneurysm (AAA) is clear, 12-19% of AAA patients have one or more first-degree relatives with an aneurysm and 4-19% is detected with ultrasound screening. OBJECTIVES: To review the genetic background of AAA. DESIGN, METHODS AND MATERIALS: Computer searches of the MEDLINE, EMBASE, SUMsearch database and the Cochrane Library and searched reference lists of English language articles concerning the genetics of AAA, candidate gene approach and linkage analysis. RESULTS: Brothers of AAA patients are at high risk to develop an AAA. The candidate gene approach was performed to detect defects in one of the components of the connective tissue, i.e. type I and III collagen, elastin and fibrillin, the inflammatory cell-derived matrix metalloproteinase, there inhibitors, auto-immune components and components related to atherosclerosis. CONCLUSION: These studies give us insight in the pathology but do not lead to the specific genetic factor(s) responsible for (familial) AAA. Considering the supposed autosomal dominant inheritance, a gene mutation in one of the structural proteins of the connective tissue is expected. In the future, linkage analysis may resolve the genetic background of AAA.

Aortic Aneurysm, Abdominal↗
PubMed1995

Genetic background and environment contribute synergistically to the onset of autoimmune diseases.

Autoimmune diseases result from the breakdown of "self" tolerance. Environmental factors appear to be responsible for triggering this errant immune response, directed against self-tissue determinants, only when a susceptible genetic background is present in an individual. Autoimmune diseases, normally characterized by their association with certain HLA alleles, also share other features: the presence of autoantibodies, autoreactive T lymphocytes, and an intermittent clinical course of exacerbations and remissions. In cases of organ-specific diseases, as well as in cases of multi-system autoimmune diseases, viruses are increasingly implicated as such environmental triggers. Current molecular biology techniques have permitted a fine dissection of the genetic background of susceptible individuals and have enabled a more complete characterization of the immunocompetent cells involved in this autoaggression. Molecular approaches will soon allow us to pinpoint the characteristics of the environmental stimuli, so that protective strategies could be formulated to spare susceptible individuals from their ill effects.

Autoimmune Diseases↗
PubMed2001

The nitrogen-induced recovery of alpha-zein gene expression in in vitro cultured opaque2 maize endosperms depends on the genetic background.

The effect of nitrogen nutrition on the accumulation of seed storage proteins has been studied in vitro by cultivating on agar media maize (Zea mays L.) endosperm explants from seeds at 10 days after pollination. The experiments were performed on various genetic backgrounds bearing different opaque2 (o2) mutant alleles and on the corresponding wild-type lines. In the seed of the o2 genotypes the high molecular weight alpha-zein polypeptides (zHs), whose transcription is Opaque2 (O2) regulated, are absent or extremely reduced. The endosperms were incubated on basal agar medium with amino acid supply. In these growth conditions, fresh and dry weights increased in both wild-type and o2 endosperms, irrespective of the genetic background. In 4 out of the 5 o2 mutant genotypes analysed we detected an accumulation of the zHs similar to the corresponding wild-type explants or seeds. However, in one of these mutants, Mo17o2R, the addition of amino acids to the culture media had no effect on the zH accumulation. We showed that the Mo17o2R behaviour is not due to a negative regulation but to the absence of putative transcription factor(s) able to regulate the zH transcription occurring in the other o2 mutants.

Journal Article↗
PubMed2003

Influence of the CBA genetic background on sperm morphology and fertilization efficiency in mice with a partial Y chromosome deletion.

Males of the B10.BR-Ydel mouse strain, with a deletion in the long arm of the Y chromosome, were backcrossed to CBA females to introduce the Ydel chromosome to the genetic background of the CBA mice. The CBA-Ydel males (sixth backcross generation) had similar symptoms to those previously described for B10.BR-Ydel males (deterioration of sperm quality and of efficiency of fertilization), but these effects were much less pronounced, showing a favourable influence of the CBA genetic background. The CBA-Ydel males produced only 12% severely misshapen spermatozoa, and mating with B10.BR females gave 100% successful fertilization. Although nearly all sperm heads were abnormal (92% versus 6% in control males), most of the spermatozoa (76%) had deformation only in the acrosomal part, that is, flat heads, which were not found in the control males. These abnormalities were analysed in detail. As shown by differential staining, the acrosomes of the spermatozoa with flat heads were deformed; 18% of these acrosomes looked damaged, and often contained a vesicle, which stained in a similar way to the acrosome but lacked the reaction for acrosomal proteinase. Electron microscopy of testis sections revealed that deformations appeared already in round spermatids as distortion of the acrosomal vesicle and asymmetrical position of the acrosomal granule; in many elongating spermatids the proximal end had a flat or concave shape, and the acrosomes contained a translucent vesicle. It is possible that the genes that are missing in the Yq deletion have some important regulatory function in the course of spermiogenesis, which may explain the various sperm defects observed in Y-del males.

Animals↗
PubMed2005

Genetic background influences immune responses and disease outcome of cutaneous L. mexicana infection in mice.

The experimental model of high-dose Leishmania mexicana infection is used frequently to study molecular mechanisms regulating Th2 response since most inbred mice regardless of their genetic background display Th2 cytokine-dependent susceptibility to L. mexicana unlike Leishmania major. Here, we analyzed the course of L. mexicana infection in BALB/c, C57BL/6 and CBA/J mouse strains using low-dose ear infection model that mimics natural transmission. Although all three strains were equally susceptible to high-dose back rump L. mexicana infection, they displayed marked differences in their ability to control parasite growth after low-dose ear infection. Leishmania mexicana-infected BALB/c mice produced high levels of Th2-associated cytokines and developed non-healing lesions full of parasites, whereas CBA/J mice preferentially produced Th1-associated IFN-gamma but low levels of IL-4, and developed small self-resolving lesions. Both BALB/c and C57BL/6 mice produced comparable amounts of IFN-gamma following L. mexicana infection, but later produced less Th2-associated cytokines, and exhibited an 'intermediate' susceptibility phenotype characterized by lesion sizes that were significantly smaller than BALB/c mice but larger than CBA/J mice. Interestingly, all three strains also showed marked differences in trafficking of macrophages, CD4+ T cells and CD8+ T cells into their lesions. Finally, we analyzed the course of low-dose L. mexicana infection in signal transducers and activators of transcription (STAT) 6-/- and STAT6+/+ BALB/c mice. We found that STAT6-/- mice mount a Th1 response, produce high levels of IL-12 and IFN-gamma and develop smaller lesions containing fewer parasites as compared with STAT6+/+ mice. Our findings demonstrate that genetic background plays a critical role in determining susceptibility of inbred mice to low-dose L. mexicana infection. Furthermore, together with our previous findings, they show that STAT6-mediated signaling is involved in mediating susceptibility to L. mexicana following both high-dose back rump and low-dose ear dermis infection.

Animals↗
PubMed1999

Functional analysis of the heterologous NSP1 genes in the genetic background of simian rotavirus SA11.

Function of rotavirus NSP1 was analyzed by using single-NSP1 gene-substitution reassortants, SKF, SDF, and SNF which have the NSP1 gene derived from human rotaviruses KU, DS-1, and canine rotavirus K9, respectively, in the genetic background of simian rotavirus SA11. The NSP1 genes from KU, DS-1, K9, and SA11 exhibited 58-76% nucleotide sequence identity to one another. No substantial difference in viral growth was observed among the reassortants and SA11. However, production of NSP1 was not detected in SNF when viral proteins were labelled with 35S-methionine during replication in MA104 cells, in contrast to SA11, SKF and SDF which exhibited evident expression of NSP1. Difference in reassortant formation was examined among the reassortant clones generated between human rotavirus strain 69M and either of SA11, SKF or SNF. Although reassortant formation rate was significantly lower in the cross 69M x SNF than the other crosses, selection rates of RNA segments from parent strain 69M in the resultant reassortants was similar among the crosses. Selectivity of homologous and heterologous NSP1 genes in SA11 background was also analyzed by mixed infection and multiple passages among the single-NSP1 gene-reassortants and/or SA11, KU NSP1 gene was selected most frequently, whereas homologous (SA11) NSP1 gene was least efficiently segregated. These results indicated that viral growth and genome segment reassortment with other viruses may not be influenced by the presence of heterologous NSP1 and its expression level, while genomic diversity of NSP1 genes might have been associated with the relative adaptability to the genetic background of SA11.

Animals↗
PubMed2005

Genetic background determines the size and structure of the endocrine pancreas.

Key parameters of the endocrine pancreas, such as islet number, islet mass, beta-cell mass, and alpha-cell mass, were studied in different strains of inbred mice to investigate the impact of genetic background on the size and structure of the endocrine pancreas. Six mice from each of seven different strains of inbred mice were included in the study. For all parameters investigated, there was a pronounced interstrain variation. ANCOVA showed that only mouse strain was statistically significant as an explanatory parameter for the number of islets. Mouse strain, body weight, and pancreas mass reached statistical significance as explanatory parameters for the islet mass, with mouse strain as the most significant predictor. These data show that genetic background is the most important predictor of both the number of islets and total islet volume. We also conclude that inbred mice could be a valuable resource to identify the genes responsible for the size and structure of the endocrine pancreas.

Analysis of Variance↗
PubMed2004

Genetic background has a major effect on the penetrance and severity of craniofacial defects in mice heterozygous for the gene encoding the nucleolar protein Treacle.

Treacher Collins syndrome (TCS) is a craniofacial disorder that results from mutations in TCOF1, which encodes the nucleolar protein Treacle. The severity of the clinical features exhibits wide variation and includes hypoplasia of the mandible and maxilla, abnormalities of the external ears and middle ear ossicles, and cleft palate. To determine the in vivo function of Treacle, we previously generated Tcof1 heterozygous mice on a mixed C57BL/6 and 129 background. These mice exhibited a lethal phenotype, which included abnormal development of the maxilla, absence of the eyes and nasal passages, and neural tube defects. Here, we show that placing the mutation onto different genetic backgrounds has a major effect on the penetrance and severity of the craniofacial and other defects. The offspring exhibit markedly variable strain-dependent phenotypes that range from extremely severe and lethal in a mixed CBA/Ca and 129 background, to apparently normal and viable in a mixed BALB/c and 129 background. In the former case, in addition to a profoundly severe craniofacial phenotype, CBA-derived heterozygous mice also exhibited delayed ossification of the long bones, rib fusions, and digit anomalies. The results of our studies indicate that factors in the different genetic backgrounds contribute extensively to the Tcof1 phenotype.

Animals↗
PubMed2005

Effect of genetic background on glycosylation heterogeneity in human antithrombin produced in the mammary gland of transgenic goats.

Glycosylation is involved in the correct folding, targeting, bioactivity and clearance of therapeutic glycoproteins. With the development of transgenic animals as expression systems it is important to understand the impact of different genetic backgrounds and lactations on glycosylation. We have evaluated the glycosylation of recombinant antithrombin produced in several transgenic goat lines, from cloned animals and from different types of lactation including induced lactations. Our results show glycosylation patterns from the protein expressed in animals, derived from the same founder goat, are mostly comparable. Furthermore, the protein expressed in two cloned goats had highly consistent oligosaccharide profiles and similar carbohydrate composition. However, there were significantly different oligosaccharide profiles from the proteins derived from different founder goats. Artificial induction of lactation did not have significant effects on overall carbohydrate structures when compared to natural lactation. The only major difference was that recombinant antithrombin from induced lactations contained a slightly higher ratio of N-acetylneuraminic acid to N-glycolylneuraminic acid and less amount of oligosaccharides containing N-glycolylneuraminic acid. The oligosaccharides from all animals were a mixture of high mannose-, hybrid- and complex-type oligosaccharides. Sialic acid was present as alpha-2,6-linkage and no alpha-1,3-linked galactose was observed. These results indicate that transgenic animals with closely related genetic backgrounds express recombinant protein with comparable glycosylation.

Animals↗
PubMed2005

Pattern of compensatory expression of voltage-dependent Ca2+ channel alpha1 and beta subunits in brain of N-type Ca2+ channel alpha1B subunit gene-deficient mice with a CBA/JN genetic background.

The Ca(2+) channel alpha(1B) subunit is a pore-forming component capable of generating N-type Ca(2+) channel activity. Although the N-type Ca(2+) channel plays a role in a variety of neuronal functions, alpha(1B)-deficient mice with a CBA/JN genetic background show no apparent behavioral or anatomical-histological abnormality, presumably owing to compensation by other Ca(2+) channels. In this study, we examined the mRNA expression of the alpha(1A), alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits in the olfactory bulb, cerebral cortex, hippocampus and cerebellum of alpha(1B)-deficient mice. We found that the mRNA expression levels of the alpha(1A), alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits were the same in the olfactory bulbs of wild, heterozygous and homozygous alpha(1B)-deficient mice. In the cerebral cortex, alpha(1A) mRNA in homozygous alpha(1B)-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits was found among wild, heterozygous and homozygous mice. In hippocampus and cerebellum, beta(4) mRNA in homozygous alpha(1B)-deficient mice was expressed at a higher level than in wild or heterozygous mice, but no difference in the expression levels of the alpha(1A), alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2) and beta(3) subunits was found among wild, heterozygous and homozygous mice. These results suggest that the compensatory mechanisms differ in different brain regions of alpha(1B)-deficient mice with a CBA/JN genetic background.

Animals↗
PubMed2002

Genetic background determines the requirement for B7 costimulation in induction of autoimmunity.

B7 costimulatory molecules play an important role in inducing autoimmunity, tumor immunity, and transplant rejection, and therapeutic manipulation of B7 is being investigated in human diseases. To determine whether B7 costimulation is essential for inducing autoimmunity on different genetic backgrounds, we backcrossed B7.1/B7.2 deficient ((-/-)) mice on to the C57BL/6 (B6) and SJL backgrounds and induced experimental autoimmune encephalomyelitis (EAE) in these mice. B7.1/B7.2(-/-) mice on the B6 background were resistant to EAE induced with MOG 35-55, whereas the SJL B7.1/B7.2(-/-) mice were susceptible to PLP 139-151 or PLP 178-191-induced EAE. The SJL B7.1/B7.2(-/-) mice had a qualitatively different lesion pattern in that they showed increased white matter vacuolation compared to wild-type SJL mice when immunized with either PLP 139-151 or PLP 178-191. (B6xSJL)F1 B7.1/B7.2(+/+) mice were susceptible to EAE whereas (B6xSJL)F1 B7.1/B7.2(-/-) mice were resistant to EAE induced with either encephalitogenic peptide. Thus, genetic background determines the B7 requirement for inducing autoimmunity. These data have important implications for developing B7-based immunotherapies for human diseases.

Abatacept↗
PubMed2001

Bone brittleness varies with genetic background in A/J and C57BL/6J inbred mice.

The contribution of genetic and environmental factors to variations in bone quality are understood poorly. We tested whether bone brittleness varies with genetic background using the A/J and C57BL/6J inbred mouse strains. Whole bone four-point bending tests revealed a 70% decrease in postyield deflection of A/J femurs compared with C57BL/6J, indicating that A/J femurs failed in a significantly more brittle manner. Cyclic loading studies indicated that A/J femurs accumulated damage differently than C57BL/6J femurs, consistent with their increased brittleness. Differences in matrix composition also were observed between the two mouse strains. A/J femurs had a 4.5% increase in ash content and an 11.8% decrease in collagen content. Interestingly, a reciprocal relationship was observed between femoral geometry and material stiffness; this relationship may have contributed to the brittle phenotype of A/J femurs. A/J femurs are more slender than those of C57BL/6J femurs; however, their 47% smaller moment of inertia appeared to be compensated by an increased tissue stiffness at the expense of altered tissue damageability. Importantly, these differences in whole bone mechanical properties between A/J and C57BL/6J femurs could not have been predicted from bone mass or density measures alone. The results indicated that bone brittleness is a genetically influenced trait and that it is associated with genetically determined differences in whole bone architecture, bone matrix composition, and mechanisms of cyclical damage accumulation.

Animals↗
PubMed1998

Preferential selection of heterologous G3-VP7 gene in the genetic background of simian rotavirus SA11 detected by using a homotypic single-VP7 gene-substitution reassortant.

Introduction of segmented genomes into virion is an important process in viral replication of rotavirus. We previously studied the assortment of the VP7 gene segment (encoding outer capsid protein VP7) in the genetic background of simian rotavirus SA11 (G serotype 3, G3) and found the preferential selection of homologous G3 VP7 gene over VP7 gene of heterologous G serotype (G1, G2 or G4). In the present study, in order to clarify whether or not VP7 gene derived from different G3 rotavirus (heterologous G3-VP7 gene) is also preferentially selected in the SA11 background, a single-VP7 gene-substitution reassortant was prepared from SA11 through multiple steps of coinfection with rotaviruses in vitro. The isolated reassortant, SNR1, possessed VP7 gene derived from canine G3 rotavirus K9 and all other gene segments of SA11 origin, and showed an identical growth characteristic to that of SA11. Amino acid sequence of K9 VP7 gene showed a high degree of identity (93.6%) to SA11 VP7 gene. In analysis by mixed infection and multiple passages of SNR1 and a single VP7 gene (with G1, G2 or G4 specificity) reassortant in the SA11 background, the G3-VP7 gene became predominant at early passage numbers. However, in mixed infection with SA11 and SNR1, homologous G3-VP7 gene (SA11-VP7 gene) was preferentially selected into progenies over heterologous one (K9-VP7 gene). These results together with our previous findings suggested that G3-VP7 gene, irrespective of origin of species, was functionally adapted to the genetic background of SA11, although the homologous gene had a better fit with other SA11 genes than did heterologous one, providing suggestions for efficaciousness of multivalent reassortant rotavirus vaccine.

Amino Acid Substitution↗