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At least 91 records · Page 5Linked to original sources
PubMed2003

Intra-farm variation of rodent infestations on poultry farms of central Argentina.

1. During the summer and winter of 1998 we monitored rodent infestation in the sheds of 9 poultry farms in central Argentina to estimate variation in rodent infestation within farms and its possible association with shed structure and farm design. 2. We observed great heterogeneity in rodent infestations, with a mean variation of 37% in the 'Rodent Infestation Index' (RII; an estimate of rodent density revealed by tracks) between sheds of the same farm. 3. In summer, the group of sheds that showed the highest RII had a higher chicken density than the group of sheds with the lowest RII. Sheds located between other sheds of the same farm showed a lower RII than sheds located beside the perimeter of the farm. 4. Our results support the hypothesis that rodents show habitat selection at both macro (farm) and microhabitat (shed) scales, and that the variables associated with these associations can change according to the scale. 5. Our observation that sheds located beside the perimeter of the farms are prone to rodent invasions reinforces our previous recommendation that farms with an efficient control of vegetation growth around their perimeter would have appreciably lower rodent infestations.

Animal Husbandry↗
PubMed1989

Seasonal patterns of rodents, fleas and plague status in the Western Usambara Mountains, Tanzania.

Field and commensal rodents were live-trapped at three villages in an active focus of plague (Yersinia pseudotuberculosis pestis) in Lushoto District, Western Usambara Mountains, Tanga Region, Tanzania, from December 1983 to November 1984. Their flea ectoparasites were collected, identified and counted. The rodent carcasses were serologically examined for specific plague antibodies and antigens, and bacteriologically examined for bipolar staining bacilli. A total of 1758 traps were set during the 12-month period and 924 animals were caught. From these, 1037 fleas were collected. Rattus rattus (L.), Praomys natalensis (Smith) and Lophuromys flavopunctatus Thomas comprised the largest proportions of the rodent population, while Dinopsyllus lypusus Jordan & Rothschild, Ctenophthalmus calceatus Waterston and Xenopsylla brasiliensis (Baker) were the dominant flea species. Rodents were most abundantly trapped during December and January. Flea indices were highest from December to May. Human plague was most active from November to March. Rodents contained plague antibodies every month except May and July, with a peak in September. Plague antigens and bipolar bacilli were detected in rodent organs during January-April. From the product of abundance and infection rate, the most prevalent rodent hosts of plague appeared to be R. rattus, Otomys angoniensis Wroughton, P. natalensis and Pelomys fallax (Peters). Continuous integrated control of rodents and fleas was recommended, reinforced by quarantine and maintenance of a surveillance service for clinical detection, diagnosis and treatment of patients in the plague endemic area.

Animals↗
PubMed1997

Experimental evaluation of rodent exclusion methods to reduce hantavirus transmission to humans in rural housing.

An experimental assessment of methods to reduce rodent infestations in rural housing was conducted in Yosemite National Park, California, Sequoia/Kings Canyon National Parks, California, and Shenandoah National Park, Virginia. During pretreatment surveys, nearly all (63 of 68) selected units had past or ongoing rodent activity inside. Active infestations were found in 58.8% of the units. Peromyscus spp. represented 91.2% of all animals caught inside housing units. Despite little harborage, rodent activity was common near housing (290 animals/2,254 trap nights). The most common species present was Peromyscus maniculatus (43-50% of all captures). This species was especially frequent (49-87% of Peromyscus captures) around the foundations of housing units. Habitat had little effect on captures. There were 1.8 Peromyscus caught per unit along the foundations of housing in modified rural settings with grass lawns compared with 1.2 Peromyscus caught per unit in sites located in mature woodlands. During autumn of 1994, randomly selected housing units were rodent proofed by sealing openings associated with chases, roof eaves, and attics with insulation and wire mesh. Housing was examined and the fauna was resampled in the spring-summer of 1995. Rodent-proofed houses were infested significantly less often (3 of 28) than control houses (13 of 36) (P = 0.02) and the intensity of infestation was lower in experimental houses (6 versus 23 mice/treatment). More than 25% of the mice trapped inside the houses had been marked outside the houses during the three-day surveys, demonstrating movement of mice adjacent to the buildings into not rodent-proofed housing. As in the previous autumn, most of the animals captured in (98.9%) and along the foundations of the houses (77.5%) were Peromyscus spp. These results demonstrate that Peromyscus frequently invade rural housing but rodent-proofing effectively eliminates or substantially reduces rodent activity.

Animals↗
PubMed1999

Hantavirus (Bunyaviridae) infections in rodents from Orange and San Diego counties, California.

During a screening program to determine the extent of hantavirus activity in Orange and San Diego Counties, California, serum samples from 2,365 rodents representing nine genera and 15 species were tested for hantavirus antibodies. A reverse transcription-polymerase chain reaction on selected seropositive rodents was used to identify the specific hantavirus. Rodents positive for Sin Nombre virus (SNV) antibodies by Western blot included 86 (9.1%) of 948 deer mice (Peromyscus maniculatus), four (1.5%) of 275 California mice (Peromyscus californicus), one (0.5%) of 196 cactus mice (Peromyscus eremicus), 51 (12.2%) of 417 harvest mice (Reithrodontomys megalotis), and five (12.5%) of 40 California voles (Microtus californicus). All other specimens tested were negative for hantavirus antibodies. There was a correlation between age and sex of the reservoir host and prevalence of SNV antibody, especially among male deer mice and harvest mice. Few seasonal trends in antibody prevalence were observed and continued maintenance of SNV and El Moro Canyon virus was found at several foci over a 4-5-year period. Isla Vista virus was also found in voles and represents the first recorded in Orange County. Microhabitat selection on the part of these rodents based on plant density, plant height, and availability of food plants may explain, to some extent, all of the hantavirus-positive foci throughout the study area over a broad geographic range and the lack of antibody-positive rodents in dense chaparral, woodland, and riparian areas. The majority of rodents positive for SNV was identified from localities along coastal bluffs and the foothills of the Santa Ana Mountains, where trap success was high and P. maniculatus represented 43% of all rodents collected. Several residential, commercial, and industrial sites exist in these areas and the potential health risk should not be overlooked. This study represents an in-depth analysis of the prevalence, host distribution, and characteristics of rodent populations infected by three hantaviruses within a small, well-defined, geographic area.

Animals↗
PubMed2006

Studies on rodents role as reservoir hosts of leishmaniasis with specical reference to their ectoparasites in Suez Governorate.

The distribution of rodents was studied in three different habitats. Seven rodent species were identified: Rattus norvegicus, R. alexandrinus, R. frugivorous, Mus musculus, Acomys russatus, Meriones sacramenti and Gerbillus pyramidum. The species distribution varied with the habitat type. The highest density of rodents was in July and August and the lowest one was in January. However, some species were collected all the year round. The rodents were investigated for the endo- and ecto-parasites. No Leishmania parasites were found. The ectoparasites were: Xenopsylla cheopis, Leptopsylla segnis and Ctenocephalides felis, Polyplax spinulos, Hyalomma dromedarii (nymph) and Echinolaelaps echidninus and Hemolaelaps glassgowi. Ecto-parasites were on rodents all year-round in domestic habitat and peridomestic habitats. In wild one, ecto-parasites activity was from March to December. The rodents' role as reservoir for L. major was experimentally studied. Rodents inoculated with L. major together with hamster and BALB-c mice developed cutaneous lesions. The active lesions, the rodents' ecological habitats and the presence of insect-vector may pave the way to an epidemic zoonotic leishmaniasis role.

Animals↗
PubMedDate not supplied

Prevalence of rodent and mongoose leptospirosis on the Island of Oahu.

Sporadic occurrences of human leptospirosis in recent years throughout the State of Hawaii have resulted in at least one death. Because of the apparent association of rodents and possibly mongooses with human leptospiral infections, a survey for leptospirosis was conducted among rodents as well as mongooses on Oahu. No such work had been recorded since a survey of rodents and mongooses for leptospirosis 31 years ago. In the current work, the prevalence of rodent and mongoose leptospirosis in the districts of Oahu was determined by the kidney-culture method. A serologic study of the rodents and mongooses subjected to kidney culturing was also conducted by use of the microscopic slide agglutination test. There were 1.2 times as many kidney culture results that were positive as serologic results. High prevalence of rodent leptospirosis were found where there was considerable rainfall or fresh surface water such as from streams. The overall leptospirosis prevalence for rodents was 23.4 percent, and for mongooses it was 23.0 percent. The Norway rat (Rattus norvegicus) had the highest infection rate, 33.3 percent, and the predominant (72.2 percent) organism in these infections was Leptospira icterohaemorrhagiae, which causes Weil's disease in man. Observations of rodent leptospirosis recorded 31 years ago were compared with results of the current study. The mongoose (Herpestes auropunctatus) is the preeminent carrier of Leptospira sejroe, a serotype that generally causes a mild form of leptospirosis in man.

Agglutination Tests↗
PubMed2000

Diversity and phylogenetic implications of CsCl profiles from rodent DNAs.

Buoyant density profiles of high-molecular-weight DNAs sedimented in CsCl gradients, i.e., compositional distributions of 50- to 100-kb genomic fragments, have revealed a clear difference between the murids so far studied and most other mammals, including other rodents. Sequence analyses have revealed other, related, compositional differences between murids and nonmurids. In the present study, we obtained CsCl profiles of 17 rodent species representing 13 families. The modal buoyant densities obtained for rodents span the full range of values observed in other eutherians. More remarkably, the skewness (asymmetry, mean - modal buoyant density) of the rodent profiles extends to values well below those of other eutherians. Scatterplots of these and related CsCl profile parameters show groups of rodent families that agree largely with established rodent taxonomy, in particular with the monophyly of the Geomyoidea superfamily and the position of the Dipodidae family within the Myomorpha. In contrast, while confirming and extending previously reported differences between the profiles of Myomorpha and those of other rodents, the CsCl data question a traditional hypothesis positing Gliridae within Myomorpha, as does the recently sequenced mitochondrial genome of dormouse. Analysis of CsCl profiles is presented here as a rapid, robust method for exploring rodent and other vertebrate systematics.

Animals↗
PubMed1998

Assessing the predictiveness of the Syrian hamster embryo cell transformation assay for determining the rodent carcinogenic potential of single ring aromatic/nitroaromatic amine compounds.

The pH 6.7 Syrian hamster embryo (SHE) cell transformation assay was used to test the morphological transformation potential of 5 rodent carcinogenic single ring aromatic/nitroaromatic amine compounds: 2-amino-4-nitrotoluene, 2,4-diaminotoluene, 2,4-dinitrotoluene, o-anisidine hydrochloride, and o-toluidine; and 5 noncarcinogenic single ring aromatic/nitroaromatic amine compounds: 2,6-diaminotoluene, 2,4-dimethoxyaniline hydrochloride, 4-nitro-o-phenylenediamine, p-phenylenediamine dihydrochloride, and HC Blue No. 2. All 5 rodent carcinogens produced significant morphological transformation in a dose-responsive manner. None of the 5 noncarcinogens yielded significant transformation at any of the doses tested. Therefore, the concordance between the pH 6.7 SHE cell transformation assay and rodent carcinogenicity for these 10 single ring aromatic/nitroaromatic amine compounds is 100%. In contrast, the concordance between the standard SHE cell transformation assay and rodent carcinogenicity for 13 single ring aromatic/nitroaromatic amine compounds was 62%. For 5 aromatic/nitroaromatic amine compounds which were tested in both standard and pH 6.7 SHE cell transformation assays (i.e., a subset of the above two databases), the concordance between the standard SHE cell transformation assay and the rodent bioassay was 40%, while the concordance between the pH 6.7 SHE cell transformation assay and the rodent bioassay was 100%. This relatively high concordance between the pH 6.7 SHE cell transformation assay and rodent bioassay results demonstrates the utility of the pH 6.7 SHE cell transformation assay for predicting the rodent carcinogenic potential of single ring aromatic/nitroaromatic amine compounds.

Aniline Compounds↗
PubMed2004

Species-specific immune response to immunization with human versus rodent A beta peptide.

Amyloid beta (A beta) immunization of amyloid precursor protein (APP)-transgenic (tg) mice with human A beta induces humoral immunity, however, the immune response to endogenous rodent A beta is unknown. Fourteen-month J20 APP-tg mice and non-tg littermates were immunized subcutaneously followed by chronic intranasal boosting with human or rodent A beta peptide and adjuvant LT(R192G). Rodent A beta-immunized APP-tg mice had anti-rodent A beta antibody levels of 257.8 micrograms/ml and those immunized with human A beta had anti-human A beta antibodies of 120.8 micrograms/ml. Non-tg littermates had anti-rodent and anti-human A beta antibody concentrations of 98.8 and 231.1 microgram/ml, respectively. Inter-species cross-reactivity was minimal. Anti-human A beta antibodies were predominately IgG1 and IgG2b, while anti-rodent A beta antibodies were equally IgG1, IgG2a, and IgG2b. Anti-human A beta antibodies recognized an epitope within human A beta1-9. Anti-rodent A beta antibodies did not stain Alzheimer's disease (AD) plaques but bound some plaques in APP-tg mice. Splenocytes proliferated modestly to their respective antigen and secreted low levels of IL-2 and IFN-gamma. Therefore, immunizing APP-tg and non-tg mice with rodent A beta resulted in a species-specific humoral response with modest T cell reactivity.

Alzheimer Disease↗
PubMed1999

Nutrition of rodents.

Access to a diet that provides adequate nutrition is one of the most important environmental factors influencing the well-being of rodent colonies. The dietary ingredient and nutrient composition, as well as the potential biological and chemical contaminant concentrations, are factors for consideration in selecting diets for a specific rodent colony. Estimated nutrient requirements have been published for the rodent species that are commonly used in biomedical research. The nutrient concentrations in adequate diets for other captive rodent species that are not used in biomedical research are more difficult to obtain. However, reasonable estimates of their nutrient requirements can be obtained by extrapolation of data from rodent species of a similar metabolic weight and size or from nutrient concentrations of diets that have a history of acceptable performance in the species of interest. Captive rodent colonies should be provided with nutritionally balanced diets with only limited amounts of succulent foodstuffs. The practice of feeding rodent colonies specific cereal grains is discouraged, since no single grain provides a balanced rodent diet.

Animal Feed↗
PubMed2004

Human and rodent cell lines showing no differences in the induction but differing in the repair kinetics of radiation-induced DNA base damage.

PURPOSE: To compare the induction and repair of radiation-induced base damage in human and rodent cell lines. MATERIAL AND METHODS: Experiments were performed with two human (normal fibroblasts HSF1 and tumour HeLa cells) and two rodent (mouse L929 and hamster CHO-K1) cell lines. Base damage was determined with the alkaline comet assay combined with the repair enzyme formamidopyrimidine-glycosylase (Fpg). Proteins were detected by Western blot. RESULTS: The induction of Fpg-sensitive sites was measured in human and rodent cell lines for doses up to 8 or 5 Gy, respectively. Comets were analysed in terms of tail moments, which were transformed into Gy-equivalents. The amount of Fpg-sensitive sites increased linearly with doses up to 4 Gy, whereby the ratio of single-strand breaks (ssb) to Fpg-sensitive sites was nearly identical for human and rodent cells with ssb:Fpg-sensitive sites=1:0.41+/-0.07 and 1:0.45+/-0.05, respectively. For doses exceeding 4 Gy, the amount of Fpg-sensitive sites did not increase further, indicating a dose limit up to which the comet assay can be used to detect Fpg-sensitive sites. Repair of Fpg-sensitive sites was studied for an X-ray dose of 4 Gy. For all four cell lines, the repair was measured to be completed 24 h after irradiation, but with pronounced differences in the kinetics. In both rodent cell lines, 50% of Fpg-sensitive sites were removed after t((1/2))=25+/-10 min in contrast to t((1/2))=80+/-20 min in the two human cell lines. The two species also differed in the level of polymerase ss with, on average, a three- to fivefold higher level in rodent cells compared with human cells. CONCLUSIONS: Repair of radiation-induced Fpg-sensitive sites was much faster in rodent than in human cells, which might result from the higher level of polymerase ss found in rodent cells.

Animals↗
PubMed1993

Comparative cytotoxic responses of cultured avian and rodent aortic smooth muscle cells to allylamine.

The present studies were designed to compare the acute cytotoxic responses of cultured avian and rodent aortic smooth muscle cells (SMCs) to allylamine (AAM), a selective vascular toxin. SMCs were isolated from male Japanese quail or Sprague-Dawley rats and established in culture by standard procedures. Cellular glutathione (GSH) content and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Exposure of avian and rodent SMCs in primary culture to AAM (0.2-200 microM) for 4 h was associated with a significant reduction in cellular GSH and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular GSH levels and enhanced the leakage of LDH in primary cultures of avian SMCs. In contrast, enhanced LDH leakage occurred without further GSH depletion in primary cultures of rodent SMCs upon exposure to AAM for 24 h. Removal of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 microM AAM, but was associated with marked elevation in cellular GSH levels and significant LDH leakage in rodent SMC cultures. The cytotoxic responses to 0.2-200 microM AAM in secondary cultures of avian SMCs were comparable to those observed in primary culture. In contrast, AAM-induced enzyme leakage did not consistently correlate with changes in GSH content in subcultured rodent SMCs. Challenge with 200 microM acrolein (ACR) for 4 h reduced the GSH content in avian, but not rodent, subcultures of SMCs. However, significant LDH leakage occurred in subcultures of both cell types upon exposure to ACR. Although hydrogen peroxide (H2O2) did not modulate GSH levels in avian or rodent cultures, leakage of LDH was observed in rat SMCs challenged with 200 microM H2O2. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 microM AAM for 24 h, but fully prevented cytotoxicity in rodent subcultures. These data suggest that potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic SMCs. These differences may contribute to the enhanced avian susceptibility to AAM-induced aortic injury in vivo.

Allylamine↗
PubMed1999

Molecular evolution of the nuclear von Willebrand factor gene in mammals and the phylogeny of rodents.

Nucleotide sequences of exon 28 of the von Willebrand Factor (vWF) were analyzed for a representative sampling of rodent families and eutherian orders, with one marsupial sequence as outgroup. The aim of this study was to test if inclusion of an increased taxonomic diversity in molecular analyses would shed light on three uncertainties concerning rodent phylogeny: (1) relationships between rodent families, (2) Rodentia monophyly, and (3) the sister group relationship of rodents and lagomorphs. The results did not give evidence of any particular rodent pattern of molecular evolution relative to a general eutherian pattern. Base compositions and rates of evolution of vWF sequences of rodents were in the range of placental variation. The 10 rodent families studied here cluster in five clades: Hystricognathi, Sciuridae and Aplodontidae (Sciuroidea), Muridae, Dipodidae, and Gliridae. Among hystricognaths, the following conclusions are drawn: a single colonization event in South America by Caviomorpha, a paraphyly of Old World and New World porcupines, and an African origin for Old World porcupines. Despite a broader taxonomic sampling diversity, we did not obtain a robust answer to the question of Rodentia monophyly, but in the absence of any other alternative, we cannot reject the hypothesis of a single origin of rodents. Moreover, the phylogenetic position of Lagomorpha remains totally unsettled.

Amino Acid Sequence↗
PubMed1991

Role of persistent, non-genotoxic tissue damage in rodent cancer and relevance to humans.

This review has focused on the importance of cellular proliferation in neoplasia induced by nongenotoxic carcinogens and has not attempted to address the mechanisms involved in the progression from the hyperplastic to the neoplastic state. Major advances in this area are likely in the next decade and should explain how cells in an abnormally high proliferative state are rendered more vulnerable either to the action of endogenous or environmental mutagens or to defects in cell reproduction, thus providing the stimulus for progression to neoplasia (165). In this review evidence has been presented to support the hypothesis that sustained tissue damage induced by nongenotoxic compounds in rodents predisposes to tumor development. The evidence has been obtained by drawing from the published findings of experimental rodent studies conducted over the past 50 years. The experience gained at various sites in the rodent including the connective tissue, liver, bladder, and forestomach shows the existence of a threshold dose for various test materials/agents, below which neither sustained tissue damage nor tumor induction occurs but above which level both effects are manifest. Taken collectively, an overall picture emerges that sustained cell proliferation renders various sites in the rodent vulnerable to tumor development. The validity of this hypothesis is of importance to the evaluation of carcinogenic risk of chemicals to humans. For those nongenotoxic carcinogens known to cause characteristically defined and sustainable tissue damage as a precursor of tumor development in rodents, it should be possible to establish a threshold dose below which both effects disappear and upon which a safety margin in humans can be based. Some limited evidence supports an association between chronic tissue injury and neoplastic development in humans. Note, however, that certain types of induced tissue damage may be rodent-specific and therefore have no relevance for humans. We conclude that the appearance of persistent tissue damage predisposes to tumor development in rodents exposed to nongenotoxic carcinogens and that systematic studies in rodents should provide a rational basis for arriving at a safety margin in humans exposed to such agents.

Animals↗
PubMed2004

Rodent Abeta(1-42) exhibits oxidative stress properties similar to those of human Abeta(1-42): Implications for proposed mechanisms of toxicity.

Alzheimer's disease is a neurodegenerative disorder associated with aging and cognitive decline. Amyloid beta peptide (1-42) [Abeta(1-42)] is a primary constituent of senile plaques - a hallmark of Alzheimer's disease - and has been implicated in the pathogenesis of the disease. Previous studies have shown that methionine residue 35 of beta(1-42) may play a critical role in Abeta(1-42)-mediated oxidative stress and neurotoxicity. Several additional mechanisms of neurotoxicity have been proposed, including the role of Cu(II) binding and reduction to produce hydrogen peroxide and the role of peptide aggregation. It has been reported that rodent Abeta is less likely to form larger beta-sheet structures, and consequently, large aggregates. As a consequence of the lack of deposition of the peptide in rodent brain, rodent Abeta has been proposed to be non-toxic. Additionally, the sequence of the rodent variety of Abeta(1-42) contains three amino acid substitutions compared to the human sequence. These substitutions include the shift of arginine 5, trysosine 10, and histidine 13 to glycine, phenylalanine, and arginine, respectively. This shift in sequence within the Cu(II) binding region of the peptide results in a decrease in the ability of the rodent Abeta peptide to reduce Cu(II) to Cu(I) compared to the human Abeta peptide. As a result of the effect of the amino acid variations on the ability of the rodent peptide to reduce Cu(II) to Cu(I) compared to the human peptide, the rodent beta has been proposed to lack oxidative stress properties. In this study, the oxidative stress and neurotoxic properties of rodent beta(1-42) [Abeta(1-42)Rat] were evaluated and compared to those of human Abeta(1-42). Both human Abeta(1-42) and beta(1-42)Rat were found to have a significant effect on neuronal DNA fragmentation, loss of neuritic networks, and cell viability. beta(1-42) Rat was found to cause a significant increase in both protein oxidation and lipid peroxidation, similar to Abeta(1-42), both of which were inhibited by the lipid-soluble, chain breaking antioxidant vitamin E, suggesting that reactive oxygen species play a role in the Abeta-mediated toxicity. Taken together, these results suggest that Cu(II) reduction may not play a critical role inbeta(1-42)Rat-induced oxidative stress, and that the oxidative stress exhibited by this peptide may be a consequence of the presence of methionine 35, similar to the findings associated with the native human beta(1-42) peptide.

Alzheimer Disease↗
PubMed1975

Recent isolations of Lassa virus from Nigerian rodents.

Rodents were trapped in the Benue-Plateau and North-Eastern States of Nigeria where Lassa fever had been reported in previous years. Eight Lassa virus strains were isolated from tissues and blood of rodents identified in the field as being of 3 different species: Mastomys natalensis, Rattus rattus, and Mus minutoides. All the infected rodents were collected in village habitats. These isolations indicate the presence of Lassa virus in wild rodents in Nigeria during periods when no human infections were evident.Prior studies in Sierra Leone have indicated that a single rodent species, M. natalensis, may be the important reservoir host of Lassa virus. Since the present study indicates that other rodent species may be involved as well, the ecology of Lassa virus may be more complicated than was heretofore supposed. In view of the importance of determining the geographic and species range of rodent hosts of Lassa virus, and because of the problems inherent in rodent identification under austere field conditions, it is urgent that further studies be conducted in the same areas of Nigeria to confirm these findings.

Animals↗
PubMed1975

The structure of rodent faunas associated with arenaviral infections.

The biogeographical examination of rodent faunas associated with arenaviruses reveals two distinct patterns. Lymphocytic choriomeningitis (LCM) virus is associated primarily with a single murid species, Mus musculus, although it is also known to cause laboratory infections in other species. On the other hand, the arenaviruses from the Western hemisphere are associated exclusively with a large and diverse group of cricetid rodents. Studies to date, although limited, have not demonstrated their association with any other rodent groups, although in South America alone at least twelve other rodent families are known. Evidence at the present time indicates that Lassa virus is only associated with a common African rodent, Mastomys natalensis. From this limited evidence it is as yet difficult to determine whether Lassa virus will follow the pattern of the South American arenaviruses, most of which are known from several species of rodents, or that of LCM virus, which appears to be associated with only a single rodent species. In this paper, the history and structure of South American, Eurasian, and African rodent faunas are described.

Africa↗
PubMed1990

Analysis of rodent platelet glycoprotein IIb: evidence for evolutionarily conserved domains and alternative proteolytic processing.

Recently, the full-length primary amino acid sequence for human glycoproteins (GP) IIb and IIIa have been derived from their respective cDNAs. Potential functional domains within these proteins have been proposed based primarily on homology with similar domains in other proteins having known biologic function. To further understand the relationship between structure and function of the platelet fibrinogen receptor, we have begun comparative studies of the human GPIIb/IIIa receptor with the corresponding rodent receptor. The rodent rGPIIb/IIIa receptor differs from the human receptor, having low affinity for R.G.D-containing oligopeptides and not binding at all to the C-terminus of the gamma chain of human fibrinogen. We describe the structure of rodent platelet GPIIb derived from a combination of peptide sequencing, and cDNA and partial genomic DNA sequence analysis. The initial transcript is 1037 amino acid residues, having 78% amino acid identity with its 1039 residue human analog. Both heavy chains have the N-terminal sequence L.N.L.D, agreeing with the consensus derived from other integrin family alpha heavy chains. All 18 cysteine residues occur at positions conserved in human GPIIb and the vitronectin receptor alpha subunit VNR alpha. The putative calcium-binding domains of the GPIIbs have a high level of amino acid identity (92%), supporting the supposition that these regions have a critical biologic role. The final 48 C-terminal amino acid residues of the heavy chain of rodent GPIIb share only 56% identity with its human counterpart, and the proposed cleavage site of human GPIIb into its heavy and light chains is not present in the rodent sequence. Although we demonstrate that rodent GPIIb is split into two subunits during its maturation, this process either involves a different recognition sequence in the rodent or occurs at a different site. Finally, partial genomic DNA sequence analysis indicates that there are at least two rodent GPIIb genes: a normal gene, containing introns in positions similar to those in the human gene, and a processed pseudogene. The human haploid genome contains only a single GPIIb gene.

Amino Acid Sequence↗