Simian Hemorrhagic Fever: Studies of Coagulation and Pathology

Abildgaard, Charles F.; Harrison, Janet; Espana, Carlos; Spangler, W. L.; Gribble, David H.

doi:10.4269/ajtmh.1975.24.537

Cited by 28 publications

(14 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1,2,22,23 Marked centrifollicular necrosis occurs in all lymph nodes, tonsil, and spleen and commonly occurs in ileal submucosa1 lymphoid nodules with SHF. EAV infection causes massive lymphoid necrosis of bronchiolar, mesenteric, cecal, and colonic lymph nodes on day 9 PE.…”

Section: Discussionmentioning

confidence: 99%

“…Nasal, fecal, and conjunctival swabs and clotted and heparinized blood were collected on the day before exposure and on days 1,4,7,14,21, and 28 PE for virus isolation (swabs, buffy coat, serum, and plasma), PRRS serum antibody determination, and complete blood counts. g Tissues and urine for virus isolation and tissue for histopathology were collected at necropsy on days 7 and 28 PE.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Experimental Porcine Reproductive and Respiratory Syndrome Virus Infection in One-, Four-, and 10-Week-Old Pigs

et al. 1994

View full text Add to dashboard Cite

Abstract. One-, 4-, and lo-week-old pigs were exposed to porcine reproductive and respiratory syndrome virus (PRRSV) to determine the effect of age on clinical signs, hematologic alterations, the onset and duration of viremia, routes of virus shedding, antibody production, and microscopic lesions produced by PRRSV isolate ATCC VR-2332. The response to PRRSV infection was similar among age groups. Fever, usually prolonged, and a marked dyspnea with cutaneous erythema when restrained for sample collection were the most consistent clinical signs. Prolonged periocular edema was unique to the l-week-old pigs. The white blood cell count was decreased on day 4 postexposure (PE) due to decreases in neutrophils and lymphocytes. The virus was isolated from buffy coats at day 1 PE and was isolated from serum, buffy coat, or plasma at each sample collection period through the end of the trial (day 28 PE). Virus was most consistently isolated from lung, lymph node, spleen, and tonsil on day 7 PE and exclusively from lymph node, spleen, and tonsil on day 28 PE. Virus was infrequently isolated from urine and fecal and nasal swabs. Consistent microscopic changes in all age groups included interstitial pneumonia and lymph node hypertrophy and hyperplasia on days 7 and 28 PE, lymph node necrosis on day 7 PE, and subacute mononuclear myocarditis on day 28 PE. Findings presented here indicate that interstitial pneumonia, lymphoid necrosis, and mononuclear myocarditis are characteristic lesions of PRRSV isolate ATCC VR-2332 infection in 1-, 4-, and lo-week-old pigs.Porcine reproductive and respiratory syndrome (PRRS), a recently emerging disease of swine, causes pneumonia and late term abortion characterized by stillborn pigs, partially autolyzed fetuses, and weak live-born pigs. [8][9][10][11][14][15][16]18,24,25 In conventional pigs, this virus causes fever, marked dyspnea ("thumping"), flulike signs, and an increase in pneumonia from opportunistic bacteria. ll,14,l6,18 Clinical signs in PRRS virus (PRRSV)-infected gnotobiotic pigs are inappetence, fever, diarrhea, hyperpnea, dyspnea, and rough hair coats.9 Clinical signs of the disease are reported to be more severe in neonatal pigs. The disease is caused by a positive-strand enveloped RNA virus closely related to lactate dehydrogenase-elevating virus (LDEV), equine arteritis virus (EAV), and simian hemorrhagic fever virus (SHF) and will probably be classified in the family Arteriviridae. 4,17,20 To determine the effect of age on disease, l-, 4-, and 10-week-old pigs were intranasally exposed to PRRSV. Hematologic alterations, onset and duration of vireFrom the Departments of Veterinary Diagnostic Medicine (Rosmia, routes of virus shedding, antibody production, and gross and microscopic lesions were evaluated. Materials and methodsAnimals. Thirty-two pigs (16 4-wk-old pigs and 16 10-wk-old pigs) and 2 sows with litters (each litter containing 9 1-wk-old piglets) were obtained from a swine herd seronegative for PRRS. The source herd was also seronegative for antibodies to pseu...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Experimental Porcine Reproductive and Respiratory Syndrome Virus Infection in One-, Four-, and 10-Week-Old Pigs

et al. 1994

View full text Add to dashboard Cite

show abstract

“…Analysis of SHFV outbreaks and limited experimental infection of macaques identified common clinical signs including fever, mild facial erythema, and edema as early as 48–72 hours post-infection (Abildgaard et al, 1975; Gravell et al, 1986; London, 1977; Palmer et al, 1968). Clinical signs indicative of initial infection developed within 72 hours post-inoculation and included depression and petechial rash (Palmer et al, 1968).…”

Section: Introductionmentioning

confidence: 99%

“…Clinical signs indicative of initial infection developed within 72 hours post-inoculation and included depression and petechial rash (Palmer et al, 1968). As the disease progressed, macaques developed facial edema, cyanosis, anorexia, adipsia, epistaxis, emesis, dehydration, melena, hematomata, retrobulbar hemorrhage and hematologic signs of coagulopathy (Abildgaard et al, 1975; Allen et al, 1968; Gravell et al, 1986; London, 1977; Palmer et al, 1968; Shevtsova, 1969a; Shevtsova and Krylova, 1971a; Tauraso et al, 1968). Clinically, SHFV-infected macaques developed increased activated partial thromboplastin time (aPTT) and prothrombin time (PT), decreased hematocrit, variations in both complete blood count (CBC) parameters and degrees of thrombocytopenia (Palmer et al, 1968).…”

Section: Introductionmentioning

confidence: 99%

Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease

Johnson¹,

Dodd²,

Yellayi³

et al. 2011

Virology

View full text Add to dashboard Cite

Simian Hemorrhagic Fever Virus (SHFV) has caused sporadic outbreaks of hemorrhagic fevers in macaques at primate research facilities. SHFV is a BSL-2 pathogen that has not been linked to human disease; as such, investigation of SHFV pathogenesis in non-human primates (NHPs) could serve as a model for hemorrhagic fever viruses such as Ebola, Marburg, and Lassa viruses. Here we describe the pathogenesis of SHFV in rhesus macaques inoculated with doses ranging from 50 PFU to 500,000 PFU. Disease severity was independent of dose with an overall mortality rate of 64% with signs of hemorrhagic fever and multiple organ system involvement. Analyses comparing survivors and non-survivors were performed to identify factors associated with survival revealing differences in the kinetics of viremia, immunosuppression, and regulation of hemostasis. Notable similarities between the pathogenesis of SHFV in NHPs and hemorrhagic fever viruses in humans suggest that SHFV may serve as a suitable model of BSL-4 pathogens.

show abstract

“…These data spawned the hypotheses that this outbreak was facilitated by shared tattoo needles used on multiple animal species in the facility and that wild African primates may be the natural reservoirs (2). Sporadic outbreaks of this "simian hemorrhagic fever" (SHF) continued to occur among captive macaques from the 1960s to the 1990s (5)(6)(7)(8). Until recently, it was believed that all SHF outbreaks were caused by a single virus, simian hemorrhagic fever virus (SHFV), of the nidoviral family Arteriviridae.…”

mentioning

confidence: 99%

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Moncla

Weiler²,

Barry³

et al. 2017

J Virol

View full text Add to dashboard Cite

Simian arteriviruses are a diverse clade of viruses infecting captive and wild nonhuman primates. We recently reported that Kibale red colobus virus 1 (KRCV-1) causes a mild and self-limiting disease in experimentally infected crabeating macaques, while simian hemorrhagic fever virus (SHFV) causes lethal viral hemorrhagic fever. Here we characterize how these viruses evolved during replication in cell culture and in experimentally infected macaques. During passage in cell culture, 68 substitutions that were localized in open reading frames (ORFs) likely associated with host cell entry and exit became fixed in the KRCV-1 genome. However, we did not detect any strong signatures of selection during replication in macaques. We uncovered patterns of evolution that were distinct from those observed in surveys of wild red colobus monkeys, suggesting that these species may exert different adaptive challenges for KRCV-1. During SHFV infection, we detected signatures of selection on ORF 5a and on a small subset of sites in the genome. Overall, our data suggest that patterns of evolution differ markedly among simian arteriviruses and among host species.IMPORTANCE Certain RNA viruses can cross species barriers and cause disease in new hosts. Simian arteriviruses are a diverse group of related viruses that infect captive and wild nonhuman primates, with associated disease severity ranging from apparently asymptomatic infections to severe, viral hemorrhagic fevers. We infected nonhuman primate cell cultures and then crab-eating macaques with either simian hemorrhagic fever virus (SHFV) or Kibale red colobus virus 1 (KRCV-1) and assessed within-host viral evolution. We found that KRCV-1 quickly acquired a large number of substitutions in its genome during replication in cell culture but that evolution in macaques was limited. In contrast, we detected selection focused on SHFV ORFs 5a and 5, which encode putative membrane proteins. These patterns suggest that in addition to diverse pathogenic phenotypes, these viruses may also exhibit distinct patterns of within-host evolution both in vitro and in vivo.KEYWORDS evolution, simian arterivirus, simian hemorrhagic fever virus, virology, within-host diversity I n 1964, acute outbreaks of a highly lethal viral hemorrhagic fever caused by a previously unknown agent swept through captive nonhuman primate research facilities in the former Soviet Union and the United States (1-4). Although the origin and

show abstract

Simian Hemorrhagic Fever: Studies of Coagulation and Pathology

Cited by 28 publications

References 0 publications

Experimental Porcine Reproductive and Respiratory Syndrome Virus Infection in One-, Four-, and 10-Week-Old Pigs

Experimental Porcine Reproductive and Respiratory Syndrome Virus Infection in One-, Four-, and 10-Week-Old Pigs

Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Contact Info

Product

Resources

About