Reovirus, Calicivirus, GIT Viruses PDF

Summary

This document provides an overview of reoviruses, caliciviruses, and gastrointestinal viruses, focusing on their characteristics, replication processes, and clinical manifestations. It describes the structure, genetics, and pathogenesis of these viruses.

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Microbiology Reoviruses, Calicivirus, and Gastrointestinal Viruses MEM, MD REOVIRIDAE ROTAVIRUS  Respiratory, Enteric, Orphan (REO)  R...

Microbiology Reoviruses, Calicivirus, and Gastrointestinal Viruses MEM, MD REOVIRIDAE ROTAVIRUS  Respiratory, Enteric, Orphan (REO)  Rota  “Wheel”  Respiratory and enteric viruses that are not associated  95% of children are infected by 3-5 years old with any known disease process  Stable at room temperature, treatment with detergents, 1. Orthoreovirus pH 3.5-10 (acidic to alkaline), survives on fomites o Mild URT Illness, GIT Illness,  Infectivity is enhanced by proteolytic enzyme such as Biliary Atresia Trypsin 2. Orbivirus / Coltivirus 1. Serotypes  based primarily on VP7 outer o Febrile Illness associated with capsid protein Members Headache and Myalgia 2. Groups  based on antigenicity of VP6 (Zoonosis) and electrophoretic mobility of genomic 3. Rotavirus Divided segments  A to G; Group A causes human o GIT Illness, Respiratory Tract Into: disease Illness (?) 3. Subgroups  determined by Complement  Non-Enveloped; Double-layered protein capsids with Fixation and depend on VP6 inner capsid dsRNA genomes (“double:double”) protein o Double-Layered Capsid + Double-Stranded RNA PATHOGENESIS genome  MOT: Fecal-Oral Route, possibly Respiratory Route  Resistant to environmental and GIT conditions  Adsorption to Columnar Epithelial Cells covering Villi of  Icosahedral with Double-Stranded Small Intestine  release of NSP4 Protein  (+) Cytolytic Segmented Genome and Toxin-Like Activity  loss of electrolytes and o Reovirus – 10 segments prevention of water re-absorption  Watery Diarrhea  o Rotavirus – 11 segments Severe Dehydration  (+) Re-assortment of Gene  NSP4 Protein Promotes: Segments  create HYBRID 1. Calcium Influx into Enterocytes Structure VIRUSES 2. Release of Neuronal Activators  Outer Capsid composed of 3. Neuronal Alteration in Water Absorption Structural Proteins  Shortening and blunting of Microvilli; Mononuclear Cell  Genomic segments encode Infiltration into Lamina Propia Structural and Non-Structural  1010 Viral Particles/gm of Stool released during disease  Proteins Maximal Shedding 2-5 days after start of Diarrhea REPLICATION  (+) outbreaks in pre-schools and daycare centers Ingestion  Upon ingestion, CLINICAL SYNDROMES there is proteolytic  Incubation Period: 48 hours cleavage of the  Self-Limited Proteolytic Cleavage of Outer Outer Capsid in the Capsid in GIT  Vomiting, Diarrhea, Fever, Dehydration GIT  (-) Fecal Leukocytes and Blood  From there, there  May be fatal in infants from developing countries and Formation of Intermediate / Infectious Viral Particle (ISVP) will be formation of infants who are malnourished and dehydrated before ISVP that will be infection ISVP release Core into released in the  Causes longer and more severe diseases compared to Cytoplasm Cytoplasm other viral antigens  Seizures and other milder  These enzymes neurological signs are common Enzymes in Core initiate mRNA within the Core will  Production using (+) Strand as initiate mRNA Template LABORATORY DIAGNOSIS production  Direct detection of viral antigens in stool  METHOD OF  Occurs in the CYTOPLASM CHOICE  dsRNA remains in the CORE  Enzyme Immunoassay  Inner Capsid with complete transcription system,  Latex Agglutination including enzymes for 5’ capping and polyadenylate  Serology – four-fold increase in Antibody titer addition PREVENTION  Virus leaves the during CELL LYSIS  Rotateq (RV5) ORTHOREOVIRUS o Oral Attenuated Live Vaccine  Mammalian Reovirus o Can be given to infants from 6 months to 2 years old  Ubiquitous  present in sewage and river water o 3 Dose before 15 weeks of age:  3 Serotypes (1, 2, 3)  identification is based on Should be completed by 8 months Neutralization and Hemagglutination-Inhibition Tests Given 6 weeks, 3 months, 5 months  Most people infected during childhood  (+) Antibodies  Rotatrix (RV1) in 75% of adults infected during childhood o Given 2 doses at age 2 months and 4 months PATHOGENESIS AND IMMUNITY COLTIVIRUS AND ORBIVIRUS  No significant disease in humans FEATURES DIFFERENT FROM OTHER REOVIRIDAE  After ingestion and proteolytic production of ISVP, binds ORBIVIRUS to M Cells in Small Intestines  transfer virus to  Outer Capsid without discernible capsomeric structure; Lymphoid Tissue of Peyer’s Patches  Replicate  (+) Inner Capsid is Icosahedral Viremia  Causes Viremia  long-lasting  (+) Humoral and Cellular Immune Response to Outer  Infects Erythrocyte Precursors without damaging them Capsid Protein  remains within the cells  protected from immune CLINICAL SYNDROMES response  (+) Viremia  Usually ASYMPTOMATIC COLTIVIRUS  Common cold-like mild Upper Respiratory Tract Illness  Causes Colorado Tick Fever  Gastrointestinal Disease  Vector: Dermacentro andersoni (Wood Tick)  Biliary Atresia  One of the most common tick-borne diseases in the US LABORATORY DIAGNOSIS  Symptoms of acute disease resemble Dengue  Assay of Viral Antigen or RNA in clinical material  Infect Vascular Endothelial and Vascular Smooth  Virus Isolation Muscle Cells and Pericytes  Weak Capillary Structures  Serologic Assays  (+) Hemorrhage  Hypotension  Shock Page 1 of 2 Microbiology Reoviruses, Calicivirus, and Gastrointestinal Viruses MEM, MD  Neuronal Infection  Meningitis and Encephalitis  MOT:  (+) Leukopenia involving both Neutrophils and o Primarily: Oral-Fecal Route Lymphocytes  HALLMARK o Airborne droplets of vomitus can cover a large radius LABORATORY  Few virus is needed  Immunofluorescence – most rapid and best technique  to start a large detection of viral antigen on surface of RBCs on Blood outbreak Smear  MOT is primarily of  Antibody Titer - specific IgM (+) 45 days after onset of Fecal-Oral Route illness  presumptive evidence of acute or very recent  Airborne particles infection from vomitus are CALICIVIRUSES capable of covering A. Norwalk a large radius B. Sapporo Viruses  Survive in chlorinated water at routine levels (up to 10 5 Groups C. Rabbit Hemorrhagic Disease Virus ppm) in freezing, heating up to 60C D. Marine Virus  Acute Gastroenteritis/Stomach Flu E. Hepatitis E  Viral Shedding: up to 2 weeks  Approximately same size as Picornaviruses  No evidence of long-term carrier  Naked, Positive Sense ssRNA Viruses DIAGNOSIS  Viruses distinguishable by Capsid morphology  Specimen: stool, vomitus, food, environmental swabs compromise function of intestinal brush border  (during outbreak) Prevent reabsorption of water and nutrients  RT-PCR, Serology  Infection results in delayed gastric emptying although  CDC recommends environmental disinfection of non- gastric mucosa is normal porous surfaces with 1000 ppm bleach solution (1 part  Cause outbreaks of Non-Bacterial Gastroenteritis bleach : 50 parts water) CLINICAL FEATURES SAPOROVIRUS  Incubation Period: 24-48 hours  Typical Morphology:  MOT: o (+) ssRNA, icosahedral, single capsid, 32 cup-like a. Fecal-Oral  water, shellfish, food service depressions b. Possible Airborne  EM: appearance of “Star of David”  e.g., Sapporo-Like  Immunity is short-lived and not protective Viruses  Antibodies develop after the first 72 hours after the  Sporadic cases and occasional outbreaks of diarrheal onset of illness illness in infants, young children, and elderly adults  Symptoms similar to Rotavirus Infection GASTROINTESTINAL VIRUSES  Norwalk and Related Viruses  Diarrhea, Nausea and ASTROVIRUSES Vomiting, especially in children; Fever in 1/3 of patients  Small ssRNA virus, non-enveloped,  Resolve within 12-60 hours round with an unbroken smooth  EM: surface o Star of David  cup-shaped on capsid surface  EM: 5- or 6-pointed star within smooth o Cuplike depression on capsid surface edge Characteristics  Typically associated with Respiratory, Vesicular,  Contain 3 structural proteins Hemorrhagic Disease, Gastroenteritis  Infect monolayers of human NOROVIRUS (NORWALK VIRUS) embryonic kidney cells without  Morphology: Atypical Morphology producing cytopathic effects  Smooth Surface  Human Serotypes: HuAstV 1-8  Small, round, structured viruses (e.g., Norwalk-like  Seen in stools from infants and young children with or Viruses) without Acute Gastroenteritis  Resistant to environmental pressure  detergents,  Agents in star-shape associated with Diarrhea in young drying, and acid children in daycare centers  Important cause of Epidemic Viral Gastroenteritis in  Symptoms similar to Norwalk but WITHOUT VOMITING adults  MOT: person-to-person via fecal-oral  Disease resolves after 48 hours, without serious  Outbreaks due to fecal contamination of seafood or consequences water  3 Genogroups Associated with Human Gastroenteritis; FASTIDIOUS ADENOVIRUS o GI, GII, and GIV  Replicates in Intestinal Cells o Since 2001, Genotype GII.4 Viruses have caused most  Adenovirus Group F Serotypes 40 and 41  Infantile Viral Gastroenteritis outbreaks worldwide Gastroenteritis  detected by electron microscopy or  Appears to undergo Antigenic Drift over time  Antigen-Based Assays, usually SUBCLINICAL responsible for GII.4 Virus  Onset of illness is manifested by Diarrhea in young child  Cellular Receptors:  May have Cough, Rhinorrhea, or Wheezing o Histo-Blood group antigens that are expressed on the  Pneumonia and Conjunctivitis have also been associated mucosal epithelia of the digestive tract with Adenovirus Conjunctivitis  A person’s secretor status is controlled by  Seen in feces of patients for a period of 4 days to 2 weeks Fucosyltransferase 2 Gene GASTROINTESTINAL DUE TO ADENOVIRUS o Secretor-Negative individuals are resistant to  MOT: Fecal-Oral Route infection with common strains of Norwalk Virus  Incubation Period: 3-10 days CLINICAL FEATURES  Age Group Affected:

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