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UMD BSCI 437 - Lecture 24: patterns of infection

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Lecture 24: patterns of infection BSCI 437Flint et al, Chapter 16General points• Infection can be– Acute– Persistent• Effects can range from– Unnoticeable– DeadlyViral life cycles- Cytopathic: rapidly kill the cell while producing a burst of new particles- Non-cytopathic: infection yields virions without causing immediate cell deathIncubation period - The time between the initial infection and the onset of disease symptoms. - Can range from a few days (cold viruses) to years (HIV) Stages of viral infection1. Primary infection- Infection of cells in the general location where virus enters.Common for example with cold viruses and Diarrhea causing viruses. Many viruses including HIV initially infect cells in the infected area. 2. Viremia- Virus enters the blood system and can be detected in the blood stream. Not all viruses do this. Some remain only localized.3. Secondary infection- Infection of other organ of cell types by the virus. Many viruses have high affinity for specific organs due to the presence of receptors or specific cell metabolic functions. Examples are infection of salivary glands by mumps virus, brain tissue by encephalitis virus, and liver tissue by hepatitis virus.Stages of viral infection – Varicella zoster infection (Fig. 16.3)• Primary infection: VZV infects via conjunctiva and upper respiratory tract• Days 0 – 3: Replicates in primary lymph nodes• Days 4 – 6: primary viremia, • Days 6 – 13: replication in liver, spleen, other organs• Day 14: infection of skin and appearance of rash. Infection of sensory ganglia and establishment of latent infectionVirulence- The ability of an infectious agent to cause disease. A relative term in the sense that it depends on the particular host that is infected and the state of that host as well as the site of infection. o Rabies and Ebola are highly virulent. o Some viruses infect animals but are virulent only when the host immune response is suppressed. Examples are certain herpes and hepatitis B virus -1-that become virulent when human hosts are treated with immunosuppressant drugs after organ transplant. General patterns of infection (Fig. 16.1)- Acute- Persistent- Latent, reactivating- SlowAcute Infections• Acute infections only detected by clinical symptoms. • Can be acutely infected but assymptomatic…subclincal.• Viruses usually produce large amounts of progeny• Rapid onset of symptoms• Rapid resolution of infection either by– Immune clearance or– DeathDefense against acute infectionsMost acute infections are rapidly resolvedLimited by the intrinsic and innate immune responsesLocalization to the immediate site of infection, Clearance by macrophages, NK cells, polymorphonuclear cells, complement.Adaptive immune response provides memory against subsequent infection.Virus-specific humoral and cellular responsesIf not quickly limited, acute infections are resolved by host deathe.g. many haemorragic viruses, severely immunocompromised patientsAntigenic variation – the viral response• Survival of acute infection  lifelong immunity to that specific virus• How is it that we get sick from other acute viruses over and over?o e.g. common cold, influenza• Answer: viruses capitalize on high rates of mutation to evolve around immuneresponse• Structural plasticity: virions that can tolerate many amino acid substitutions yetremain infections. o Rhinoviruses and Influenzaviruses are incredibly structurally plastic.o Limits ability to make effective vaccines• Many viruses are not structurally plastic: e.g. poliovirus. One vaccination canconfer lifelong immunityStructural plasticity: Antigenic variationThe immune system detects “epitopes” on “antigens”: structural features of molecules• Antigenic variation: o Changes in the epitopes of viral proteins that are presented to the immunesystem.-2-• Antigenic drift: o Appearance of virions with slightly altered surface proteins followingpassage in the natural host. o An evolutionary process where natural selection is driven by the hostimmune response• Antigenic shift: o A major change in a surface protein as a gene encoding a completely newsurface protein is acquired. o Results from coinfection of one host with two different viral serotypes. o Due to reassortment of genes among two or more viruses. o Very commonly seen with viruses having segmented genomes. o Reassortment and recombination of blocks of genetic information result inviral hybrids that are immunologically new to the host.Acute infections and Public HealthAcute infections are commonly associated with epidemicse.g. polio, influenza, measles, common coldMain problem: by the time symptoms emerge, the patient has passed on the infectionDifficult to control in large populations and crowded environmentse.g. work, daycare, dormsEffective antiviral drug therapy requires early intervention, safe drugs with few sideeffects…..not really practical for acute infections.Cost: 90% of outpatient visits due to self-limiting acute viral infections.Persistant Infections. Four general classes. 1) Infection by viruses which actively produce large amounts of progeny, but whichcause little cytopathology.2) Infection by normally lytic virus but in which the extent of virus multiplication issomehow limited, so that the yield of virus is small.3) Limitation of reinfection by various viral and cellular factors, so that the proportionof infected cells in the total cell population remains small but constant. - Viral factors tend to be decreased virulence, and interference of virusproduction by defective interfering particles. - Cellular factors include differences in permissiveness to infection/virusreplication, and immune surveillance.4) Chromosomal integration of proviral genomes - Result in “silent” infections, infrequent or constant rounds of low level, and onlyslight production of cytopathic virus.Some persistent viral infections of humans (see Table 16.2)VIRUS SITE OF PERSISTENCE CONSEQUENCEAdenovirus Adenoids, tonsils, lymphocytes None knownEpstein-Barr B-cells, nasophayngial epithelia Lynphoma, carcinomaH.Cytomegalovirus Kidney, salivary gland, WBCs? Pneumonia, retinitisHepatitis B virus Liver, lynphocytes Cirrhosis, liver cancer-3-Hepatitis C virus Liver Cirrhosis, liver cancerHIV CD4+ T-cells, macrophates, microgliaAIDSHSV 1 and 2 Sensory and


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