lecture 5 Flashcards
what are two components if viral diseases?
effects of replication on the host
effect of host response on virus and host
asymptomatic infections contribute to _____ and to ____
seroprevalence— frequency of individual who are positive form a pathogen based on antibodies
virus transmission
what happens when infections prevented or abortive?
-viron never finds a living cell to infect
-inactivated by the host
-never infects more than a cell or two at site of infection
what is a disease co factor?
-replication contributes to an environment in which another microbe causes the disease
-influencza pneumonia
what are viral disease that require a co factor?
viral disease requires an envoriment generates by another microbe
-kaposi sarcoma
what are barriers that make organism infectious dose higher than pfu?
what are some variables that make each persons getting a disease harder/easier?
what is TCID?
skin, mucus layers
genetics
host antiviral deference
viral virulence
social behavior
age
tissue culture infectious dose
how do some virus alter host replication?
-commandeer transcription or translation machinery
-stimulate quiescent cells to divide
what does measles kill?
HIV?
what can happen after recovering from it and how?
kills B cells, HIV is CD4+ T cells
-can have immune amnesia due to reduced antibody repertoire can leave susceptibility to previous vaccine or infection
why is having ds RNA bad for the virus?
how does this affect the host?
dsRNA triggers interferon (IFN), which is an inhibitor of translation–> leads to cell death
-virus spread is halted + can lead to inflammation
massive inflammatory response
why is IFN system dangerous?
what does every viral infection lead to?
large IFN lead to fever, chills, nausea, malaise
-IFN production, why flu like symptoms are so common
what are acute infections?
what is viremia?
-virus enter the body replicates & causes disease (or not)
-can be localized or spread in the body
-cleared from the body or person dies
-ends with no infectious virus remaining in the person, often immunological memory
virus in the blood
what are persistent infections?
what are chronic + latent?
enter a body cell & causes disease or not
-it is not cleared from the body
-virus remains in body after disease revolves
chronic: Hep B–> infectious is released from the host with no symptoms after initial infection
latent: herpres–> after initial infection virus is maintain in the neurons & non infectious state, can be reactived
how does covid enter the cell?
spike protein binds angiotensin converting enzyme (ACE2) on host
protease cleavage drives fusion (TMPRSS2)
what factors can intiation of viruses?
-cold increases density of attachment for receptor
-smoking can expand cells that express ACE2 (COVID)
-ACE inhibitors can upregulate ACE2
how does delayed IFN 1 signaling work in COVID?
allows virus to reach higher titer
leads to a later inflammatory response –> causes disregualted IMM response
how are PAMPS on dsRNA viruses detected?
what are parts of innate defense system?
because -RNA is templated by +RNA, vice verse, so has a dsRNA that is recognized
cytokines, pattern detectors, sentinel cells, complement
what are features that corona have that evades immune response ?
forms interconnected double membrane intracytplasmic vesicles (RTC)
encodes many accessory proteins/ factors that limit interferon response —->
when are virus titers the highest and lowest in SARS?
-highest before disease symptoms occurs–> easier to detect before patient is sick
-titers are lower as disease progresses–> suggesting antivirals effective only after earlier stage
how is polio passed?
howdies it replicate?
what are the symptoms like?
when does it shed?
fecal oral route
replication at site of infection in oropharynx or SI —> then decimates to secondary sites
non detectable– 90-95%
after 3 months
forever immunity
what is dengue virus?
what happens Upon reinfection, and are you immune forever and why not?
RNA virus—falvivirus
most common vector born virus
-dengue hemmorage fever–> no
-because of antibody depends enchancement function —–>interactions with FcyR on monocytes
