Virology Quiz #4B

Front 1

herpes virus (virion)

Back 1

enveloped
single molecule of linear dsDNA
icoadehdral nucleocapsid

Front 2

herpes virus (site of nucleocapsid assembly)

Back 2

nucleus

resulting in a nuclear inclusion body

Front 3

herpes virus (replication steps)

Back 3

a) an extracellular virion adsorbs to a susceptible cell
b) virion envelope fuses and penetrates the plasma membrane of the host cell
c) nucleocapsid goes to the nucleus and releases its DNA into the nucleus
d) the DNA becomes circular
e) synthesis of mRNA, viral proteins, and viral DNA takes place
f) progeny nucleocapsids are assembled in the nucleus, large arrays of nucleocapsids result in characteristic nuclear inclusion bodies
g) virus-encoded glycoproteins inserted into nuclear membrane and plasma membrane
i) virus encoded glycoproteins in plasma membrane can result in cell fusion to produce multinucleate giant cells (compare measles)

Front 4

in replication of Herpes Virus, when does the DNA cyclize?

Back 4

after the nucleocapsid goes to and releases its DNA into the nucleus

[DNA becomes circular]

followed by mRNA synthesis, viral proteins and viral DNA

Front 5

where are herpes nucleocapsids assembled?

Back 5

in the nucleus

Front 6

Herpes virus (inclusion bodies)

Back 6

large arrays of nucleocapsids, found in the nucleus result in characteristic nuclear inclusion bodies

Front 7

why can herpes virus result in multinucleate giant cells

Back 7

virus-encoded glycoproteins in the plasma membrane can result in cell fusion to produce multinucleate giant cells

Front 8

how are infectious herpes virus virions produced?

Back 8

by nucleocapsid budding through the nuclear membrane

Front 9

single most important biological characteristic of herpes viruses

Back 9

LATENCY: herpes viruses are not eliminated on recovery from primary infection, but remain in a clinically "latent" state that can subsequently result in recurent disease

Front 10

how is the herpes virus maintained in small populations?

Back 10

patients with latent infection may sporadically produce infectious virions (while remaining asymptomatic)

this latent state-recurrent infection allows parent --> child transmission and maintenance of virus in small populations

Front 11

Number of herpes viruses known to infect humans

Back 11

8, (5 to be considered in detail:
Herpes simplex virus type-1
Herpes simplex virus type-2
varicella-zoster virus
cytomegalovirus
Epstein Barr (EB) virus)

Front 12

How are Herpes Simplex type-1 and type-2 distinguised

Back 12

closely related antigenically

distinguished by type-specific monoclonal antibodies of PCR

Front 13

viruses that remian latent in sensory ganglion cells

Back 13

Herpes simplex type-1
Herpes simplex type-2
and Varicella-zoster viruses

(when infection is reactivated, virus makes its way to skin by neural pathway causing unilateral skin lesions, whereas primary lesions are often bilateral)

Front 14

populations affected by recurrent herpes simplex type 1 and type 2 and varicella-zoster virus infections

Back 14

seen in immunologically normal persons, pathology more severe in immunosuppressed

Front 15

latent EB virus is found

Back 15

within B lymphocytes

Front 16

latently infected cell type in cytomegalovirus infection

Back 16

uncertain

Front 17

recurrent disease (w/ EB and cytomegalovirus) almost entirely seen in what population

Back 17

immunosuppressed patients

Front 18

Herpes Simplex Type 1 (primary infection)

Back 18

often subclinical

virions produced at site of initial infection infect the sensory nerves there and infection ascends the nerve (probably in the form of nucleocapsids) to establish a latent infection in the sensory ganglion that corresponds to the initial site

some infants get somatitis with vesicles throughout the mouth

other sites of primary infection (nose, eyes, fingers, etc.)

Front 19

Herpes Simplex Type 1 (incubation period)

Back 19

1-2 weeks

Front 20

Herpes Simplex Type 1 (latent virus isolated from...)

Back 20

sensory ganglia

Front 21

Herpes Simplex Type 1 (reccurent infection begins when...)

Back 21

extensive viral multiplication is "turned on" in the nucleus of a senosry ganglion cell

resulting virions are transported down the axon to the cutaneous site (corresponding to the primary infection)

local infection with vesicular lesions (cold sores) results

cold sores are self-limiting local lesions

Front 22

cold sores in Herpes Simplex Type 1

Back 22

are self-limiting local lesions

produce many infectious virions

Front 23

what prevents disseminated infection in recurrent Herpes Simplex Tyle 1 infection

Back 23

circulating Ab already present as result of primary infection

Front 24

small amounts of infectious virus sporadically released in latent Herpes Simplex Type 1 do what?

Back 24

do NOT produce lesions

Front 25

what can activate latent Herpes Simplex Type 1 infections to produce cold sores?

Back 25

fever, UV light, emotion

Front 26

Herpes simplex type 2 (disease)

Back 26

STD with lesions on the genitalia

Front 27

Herpes simplex type 2 (population infected)

Back 27

seroconversion is seen in populations after the age of puberty

currently ~20% of US population is seropositive (latently infected)

Front 28

Herpes simplex type 2 (primary infection)

Back 28

may be severe with multiple BILATERAL lesions

but many are asymptomatic

reulsts in a latent infection of the sensory ganglia cells that innervate the genitalia (SACRAL GANGLIA)

Front 29

Herpes simplex type 2 (incubation period)

Back 29

1-2 weeks

Front 30

Herpes simplex type 2 (characteristics of recurrent disease)

Back 30

fewer lesions, generally unilateral

Front 31

Herpes simplex type 2 (how is recurrent disease prevented)

Back 31

chemotherapy with acyclovir

Front 32

most persons latently infected with Herpes simplex type 2

Back 32

sporadically produce small amts of infectious virus

even though they have no overt lesions

Front 33

Herpes simplex type 2 (transmission)

Back 33

Sexual Transmission
Perinatal transmission (via virions in vaginal secretions of latently or acutely infected mother)

Front 34

neonatal herpes simplex

Back 34

caused by perinatal infection
systemic disease
appears ~6 days pp
often fatal
most organs are invaded by the virus in neonatal disease
marked by HEPATO-ADRENAL NECROSIS

highest risk of perinatal infection and fatal outcome when mother has acute primary Herpes Simplex Type 2 infection

Front 35

HEPATO-ADRENAL NECROSIS

Back 35

destruction of liver and adrenals characteristic of neonatal herpes simplex

Front 36

prevention of neonatal herpes simplex

Back 36

if vaginal lesions are present before delivery, strong indication for C-section

Front 37

most common cause of sporadic (non-epidemic) encephalitis

Back 37

Herpes simplex (mostly type 1)

route to CNS is probably neural

Front 38

Herpes simplex encephalitis is seen in what patient populations

Back 38

primary infection
and
in patients with history of recurrent lesions

Front 39

Herpes simplex encephalitis (site of infection/symptoms)

Back 39

temporal lobe is most commonly infected, may give rise to temporal lob symptoms

(auditory or olfactory hallucinations)

Front 40

Herpes simplex encephalitis (diagnosis)

Back 40

formerly required biopsy

now PCR detection of herpes simplex DNA in CSF

rapid diagnosis is important because chemo is available (acyclovir)

Front 41

Herpes simplex encephalitis (treatment)

Back 41

chemotherapy with acyclovir

sometimes administered on clinical suscpicion of herpes simplex encephalitis

Front 42

HERPES SIMPLEX KERATITIS

Back 42

herpes infection of the eye can lead to keratitis affecting:
the conjunctiva, eyelids, and cornea

Front 43

HERPES SIMPLEX KERATITIS (typical presentation)

Back 43

unilateral "red eye" with a variable degree of pain or ocular irritation

often associated with photophobia

Front 44

HERPES SIMPLEX KERATITIS (complications, prognosis)

Back 44

can spread to deeper levels of the eye and cause permanant damage

risk of corneal damage

Front 45

HERPES SIMPLEX KERATITIS (treatment)

Back 45

topical trifluridine or systemic acyclovir

Front 46

Varicella-Zoster Virus (primary infection)

Back 46

chicken pox

Front 47

Varicella-Zoster Virus (epidemics)

Back 47

winter-spring epidemics in children are seen every few years

Front 48

Varicella-Zoster Virus (site of primary infection)

Back 48

by way of respiratory tract, with subsequent viremia

Front 49

Varicella-Zoster Virus (incubation period)

Back 49

2-3 weeks

Front 50

Varicella-Zoster Virus (symtoms)

Back 50

fever and rash appear after 2-3 week incubation period

lesions are small itchy vesicles

characteristically lesions are in different states of developmentin the same area of skin

Front 51

Varicella-Zoster Virus (transmission)

Back 51

spread probably spread primarily by viruses shed from skin lesions

virus-containing vesicles in the mucosa rupture shorly after they form

shed virus from respiratory tract may also spread the infection

Front 52

Varicella-Zoster Virus (in patients with impaired immune response)

Back 52

get a severe and often fatal chicken pox on primary infection

if exposed can be passively immunized with IgG from donors with high known titers of neutralizing Ab (VZIG: Varicella-Zoster Immune Globulin)

less common now, bc available vaccine and chemotherapy and chemprophylaxsis with acyclovir works well

Front 53

VZIG

Back 53

Varicella-Zoster Immune Globulin:

IgG from donors known to have high titers of neutralizing Ab to Varicella-Zoster virus

before Varicella-Zoster Virus vaccine and effective chemotherapy was used to prevent severe/fatal infections in immune compromised patients

Front 54

CONGENITAL VARICELLA SYNDROME

Back 54

rare (0.5-2%) fetal infection, when pregnant mother is infected with Varicella-Zoster Virus in first or early 2nd trimester

characterized by limb atrophy, scarring of skin on the affected limb

MUCH LESS COMMON THAN congenital cytomegalovirus infection

Front 55

Latent infections with Varicella-Zoster Virus are established where?

Back 55

sensory ganglia

(same as with herpes simplex virus)

Front 56

ZOSTER

Back 56

(aka SHINGLES) disease resulting from reactivation of latent Varicella-Zoster infection

virions move down the axons, produce vesicular lsions at cutaneous site

unilateral, dermatomal distrubution

(may produce pain before lesions appear)

Front 57

SHINGLES

Back 57

(aka Zoster) disease resulting from reactivation of latent Varicella-Zoster infection

virions move down the axons, produce vesicular lsions at cutaneous site

unilateral, dermatomal distrubution

(may produce pain before lesions appear)

Front 58

Post-Herpetic Neuralgia

Back 58

severe local pain at sites of healed lesions after recovery from Zoster (shingles)

adverse outcome increases with age at which the zoster attack takes place

Acyclovir given in the first 1-2 days can reduce the risk of post-herpetic neuralgia

Front 59

Post-Herpetic Neuralgia (prevention)

Back 59

Acyclovir given in the first 1-2 days of Zoster infection can reduce the risk of post-herpetic neuralgia

Front 60

dermatomal distribution of Zoster

Back 60

patients who get zoster are seropositive as a result of original chicken pox, Ab prevents viremic spread and results in this distribution

Front 61

Disseminated Zoster

Back 61

virus is spread by viremia and produces lesions beyond the original dermatome

immunsosuppressed patients at risk

disseminated disease can be treated with acyclovir

Front 62

Zoster characterized by:

Back 62

monocyte infiltration of the involved ganglion

pain that may precede the cutaneous lesions

Front 63

Zoster (population affected)

Back 63

all ages are affected, but..

attack frequency increases with age after 50 (probably related to age-related decline in cell-mediated immunity)

higher incidence also seen in those with reduced cell-mediated immunity (AIDS, anti-cancer drugs, other immunosuppresive drugs)

Front 64

Zoster vesicles contain what?

what can they be the source of?

Back 64

vesicles contain virus

a case of zoster may be the source of a chicken pox epidemic

Front 65

explain survival of VARICELLA ZOSTER virus in small populations

Back 65

a case of zoster can cause a chicken pox epidemic

latent/recurrent infection resultant transmission

Front 66

Ab titers in patients recovered from zoster

Back 66

VERY HIGH antiviral Ab titers

Front 67

VARICELLA-ZOSTER Vaccine

Back 67

live-attenuated vaccine is available and recommended for routine pediatric use

vaccine reduces clinical infections by 85% and reduces severe infections by 97%

Front 68

CYTOMEGALOVIRUS (reason for name)

Back 68

infected cells are much enlarged

and have nuclear inclusion

Front 69

CYTOMEGALOVIRUS (primary infections)

Back 69

before puberty-- usually subclinical

teens/adults-- mono-like syndrome (but with negative heterophile test)

Front 70

CYTOMEGALOVIRUS (incubation period)

Back 70

difficult to measure
probably bt 3-12 weeks

Front 71

CYTOMEGALOVIRUS-caused mononucleosis-like syndrome

seen in:

Back 71

primary cytomegalovirus infection

or as post-blood-transfusion complication

Front 72

CYTOMEGALOVIRUS (transmission)

Back 72

requires close contact

viruses excreted in naso-pharyngeal fluid, semen, urine, and vaginal secretions

breast milk (40% transmission by seropositive nursing moms, probably due to recurrent asymptomatic infection)

person-to-person transmission is common in nursery schools

Front 73

CYTOMEGALOVIRUS (infection of nursing infants)

Back 73

40% risk of infection by seropositive mothers who breast-feed for several months

infection of nursing infants general ASYMPTOMATIC

Front 74

person-to-person transmission of this virus is common in nursery schools

Back 74

CYTOMEGALOVIRUS

Front 75

CONGENITAL INFECTION with CYTOMEGALOVIRUS

Back 75

realtively common

symptoms of maternal infection are unknown (subclinical?)

spectrum of signs in sypmtomatic congenital disease:
a. microcephalic mental retardation with intracerebral calcifications
b. neuro-sensory deafness
c. jaundice, enlarged liver/spleen
d. anemia

Front 76

incidence of symptomatic congenital cytomegalovirus infections in the US

Back 76

~4,000/year

CMV is the most frequent viral congenital infection now that rubella vaccine has reduced the incidence of rubella

Front 77

primary cause of congenital CMV

Back 77

nearly all congenital malformations result from a primary maternal infection

however, fetal infection can follow either primary infection or (asymptomatic) recurrent viremia in a latently infected mom

Front 78

immune response of fetus infected with CMV

Back 78

makes anti-CMV IgM

after birth anti-CMV IgG is also made

virus excretion continues for years just as in congenital rubella

Front 79

best method of CMV detection in neonates

Back 79

urine

Front 80

treatment of congenital CMV

Back 80

neonates treated with ganciclovir have improved outcome:
test of hearing
resolution of hepatitis
and cognitive dvpt

Front 81

CMV vaccine

Back 81

live virus vaccine is being used experimentally

Front 82

Recurrent disease caused by CMV is seen only when:

Back 82

immune response is defective (immunosuppressive therapy, luekemia, Hodgkins disease, etc..)

such patients get generalized (sometimes fatal) infection (pneumonitis and hepatitis)

Front 83

AIDS patients have higher incidence of what diseases caused by CMV?

Back 83

retinitis and gastroenteritis

Front 84

best treatment for all CMV infections

Back 84

GANGICLOVIR

(acyclovir is not used for CMV infections)

Front 85

CMV (in transplantation)

Back 85

major problem in organ transplants when the donor is seropositive and the recipient is seronegative)

transplanted organ generally contains latently infected cells

Front 86

EB [EPSTEIN-BARR] VIRUS

Back 86

most common cause of infectious mononucleosis

Front 87

MONONUCLEOSIS

Back 87

disease of teenagers and young adults

infection in young children is subclincal

virus is probably transmitted primarily by saliva transfer during kissing

Front 88

MONONUCLEOSIS (symptoms)

Back 88

fever, sore throat, lymphadenopathy

incubation period is 4-6 weeks

acute HIV infection may closely mimic this clinical presentation

Front 89

MONONUCLEOSIS (blood contains..)

Back 89

"abnormal" lymphocytes

cytotoxic T-lymphocytes produced in high numbers to attack the circulating B-lymphocytes that are infected with EB virus

Front 90

MONONUCLEOSIS (diagnostic test)

Back 90

detects short term increase in heterophile Ab to sheep red cells

heterophile Ab is presumably induced by an EB virus antigen that happens to cross-react with sheep red cells

heterophile Ab does NOT neutralize EB virus

Front 91

heterophile Ab

Back 91

induced by an EB virus antigen

but does NOT neutralize EB virus

happens to cross-react with sheep red cells

provides a cheap diagnostic test for mononucleosis

Front 92

What dose EB virus do to lymphocytes

Back 92

"Transforms" lymphocytes making them into actively dividing cells

a rare human mutation blocks the cell-mediated immune response to EB virus (resulting in fatal lymphoproliferative disease)

Front 93

fatal lymphoproliferative disease

Back 93

caused by EB infection in individuals with a rare mutation that blocks the cell mediated immunse response to EB

Front 94

proof that EB virus is the most common cause of mononucleosis

Back 94

obtained by cohort analysis

(remember CMV also causes infectious mono, but with (-) Heterophile Ab Test)

Front 95

compare antibody to EB with heterophile Ab

Back 95

Ab to EB virus rises during course of infectious mononucleosis (patients seroconvert) Ab continues to be made

Whereas heterophile Ab rapidly disappears

Front 96

Procedure equivalent to virus isolation of EB virus

Back 96

virus-producing B-lymphocytes can be cultured during acute disease

Front 97

Where is EB virus found?
Where is it produced?
When is it produced?

Back 97

found in the saliva
probably produced by lymphoid cells in oro-pharynx
virus production may continue for months after the disease is over

Front 98

Persons latently infected with EB

Back 98

produce subclinical levels of virus production

Front 99

oral hairy leucoplakia

Back 99

one recurrent infection of EB virus

seen when immune response is compromised

common in AIDS patients

characterized by whitish patches on the tongue or buccal mucosa

Front 100

consequences of latent EB virus in immunocompormised patients

Back 100

lymphoproliferative disease that occurs when virus-transformed B cells grow uncontrolled and these can develop into tumors

and other EB virus-related malignancies

Front 101

HUMAN HERPES VIRUS 6

Back 101

causes a systemic infection with rash (roseola infantum) in infants

most infected infants do not get the rash, but do have a very high fever

Front 102

HUMAN HERPES VIRUS-7

Back 102

close relative of HUMAN Herpesvirus-6 and has not been firmly associated with any disease

Front 103

HUMAN HERPES VIRUS-8

Back 103

was recently discovered and is a probably cuase of Kaposi's sarcoma

Front 104

HERPES SIMPLEX TYPE 1
(usual primary infection)
(usual recurrent infection)

Back 104

Primary: subclinical or stomatitis

Recurrent: cold sore

Front 105

HERPES SIMPLEX TYPE 2
(usual primary infection)
(usual recurrent infection)

Back 105

Primary: subclinical or vesicles on genitalia

Recurrent: vesicles on genitalia

Front 106

VARICELLA-ZOSTER
(usual primary infection)
(usual recurrent infection)

Back 106

primary: chicken pox

recurrent: zoster (shingles)

Front 107

CYTOMEGALOVIRUS
(usual primary infection)
(usual recurrent infection)

Back 107

primary: usually subclinical but causes fetal malformation;

teenagers and older may get heterophile-negative mononucleusis

recurrent: oral hairy leukoplakia or tumors when immune response is compromised

Front 108

why is selective chemical inhibition of viruses difficult?

Back 108

they are dependent on their host cells for most biochemical rxns.

Front 109

why do we have better chemotherapy for herpes viruses than for other virus groups?

Back 109

viruses with larger genomes have more potential targets for drug therapy

Front 110

mechanism of antivirals for herpesviruses

Back 110

only inhibit virus replication, and therefore disease associated with replication

they do NOT eradicate the latent infection, or diseases associated with latency (eg tumors caused by EBV)

Front 111

Acyclovir

Back 111

best available durg for systemic infections with:
HERPES SIMPLEX VIRUS
or VARICELLA-ZOSTER

an analogue of deoxyguanosine (a nucleotide that is phosphorylated by herpes viral thymidine kinase, but not host thymidine kinase)

phosphorylated by herpes thymidine kinase and then converted by host cell enzymes to the triphosphate, which is incorporated into DNA and blocks further incorporation of nucleotides

Front 112

ACYCLOVIR

Back 112

treats: systemic infections with HERPES SIMPLEX or VARICELLA-ZOSTER viruses

mechanism: analogue of deoxyguanosine, phosphorylated by herpes thymidine kinase, but not host thymidine kinase

converted to chain-terminating triphosphate by host

bc host does not phosphorylate- only terminates DNA synthesis in herpes infected cells

Front 113

GANCICLOVIR

Back 113

treats: CMV infections

mechanism: related to acyclovir analog of deoxyguanosine, phosphorylated by herpes thymidine kinase, but not host thymidine kinase

converted to chain-terminating triphosphate by host

bc host does not phosphorylate- only terminates DNA synthesis in herpes infected cells

Front 114

TRIFLURIDINE

Back 114

useful for recurrent keratitis (infection of cornea) can be applied LOCALLY to the eye

mechanism: incorporated into DNA, causes lethal replication errors AND inhibits thymidylic acid synthestase of the host cell

cells of the cornea have a very small amount of DNA synthesis and thus are not affected by the drug CANNOT BE USED FOR SYSTEMIC HERPES INFECTIONS (more rapid rates of DNA synthesis and high thymidine kinase activity= sensitive to trifluridine)

recall that herpes simplex infection recurr at site of primary infection

if that site was the eye, recurrent keratitis will result- common cause of blindness

Front 115

ADENINE ARABINOSIDE

Back 115

mechanism: an analog of deoxyadenosine, phosphorylated by host cell enzymes to make adenine arbinoside triphosphate, incorporated into viral DNA by viral DNA polymerase, blocks further DNA synthesis (CHAIN TERMINATING ANALOGUE)

useful in HERPEs SIMPLEX ENCEPHALITIS and in some immunosuppressed patients with ZOSTER

largely supplanted by acyclovir

Front 116

FOSCARNET

Back 116

treats: (alternative to ganciclovir) for CMV infections

mechanism: analog of pyrophosphate
inhibitor of herpes DNA polymerase, has much less effect on DNA of human cells

Front 117

AEROSOLIZED RIBAVIRIN

Back 117

used to treat RSV pneumonia in infants

(efficacy uncertain)

Front 118

ALPHA INTERFERON (for months)

Alpha interveron + Ribavirin

Back 118

drug used to treat chronic hepatitis caused by HCV

Front 119

ALPHA INTERFERON LAMUVINDINE

Back 119

used to treat chronic heptatitis caused by HBV

Front 120

AMANTIDINE [RIMANTIDINE]

Back 120

used to treat INFLUENZA A (only A)

Front 121

OSELTAMIVIR [zanamivir]

Back 121

used to treat all influenza (A, B and C)

Front 122

ACYCLOVIR

Back 122

used to treat all severe primary infections with herpes simplex virus

also used prophlactically to reduce the incidence of recurrent herpes simplex infection, espeically genital and corneal (keratitis) lesions

Front 123

TRIFLURIDINE or ACYCLOVIR

Back 123

used to treat recurrent herpes simplex keratitis (non retinitis- note the anatomical difference)

Front 124

why do we have better chemotherapy for herpes viruses than for other virus groups?

Back 124

viruses with larger genomes have more potential targets for drug therapy

Front 125

mechanism of antivirals for herpesviruses

Back 125

only inhibit virus replication, and therefore disease associated with replication

they do NOT eradicate the latent infection, or diseases associated with latency (eg tumors caused by EBV)

Front 126

Acyclovir

Back 126

best available durg for systemic infections with:
HERPES SIMPLEX VIRUS
or VARICELLA-ZOSTER

an analogue of deoxyguanosine (a nucleotide that is phosphorylated by herpes viral thymidine kinase, but not host thymidine kinase)

phosphorylated by herpes thymidine kinase and then converted by host cell enzymes to the triphosphate, which is incorporated into DNA and blocks further incorporation of nucleotides

Front 127

ACYCLOVIR

Back 127

treats: systemic infections with HERPES SIMPLEX or VARICELLA-ZOSTER viruses

mechanism: analogue of deoxyguanosine, phosphorylated by herpes thymidine kinase, but not host thymidine kinase

converted to chain-terminating triphosphate by host

bc host does not phosphorylate- only terminates DNA synthesis in herpes infected cells

Front 128

GANCICLOVIR

Back 128

treats: CMV infections

mechanism: related to acyclovir analog of deoxyguanosine, phosphorylated by herpes thymidine kinase, but not host thymidine kinase

converted to chain-terminating triphosphate by host

bc host does not phosphorylate- only terminates DNA synthesis in herpes infected cells

Front 129

TRIFLURIDINE

Back 129

useful for recurrent keratitis (infection of cornea) can be applied LOCALLY to the eye

mechanism: incorporated into DNA, causes lethal replication errors AND inhibits thymidylic acid synthestase of the host cell

cells of the cornea have a very small amount of DNA synthesis and thus are not affected by the drug CANNOT BE USED FOR SYSTEMIC HERPES INFECTIONS (more rapid rates of DNA synthesis and high thymidine kinase activity= sensitive to trifluridine)

recall that herpes simplex infection recurr at site of primary infection

if that site was the eye, recurrent keratitis will result- common cause of blindness

Front 130

ADENINE ARABINOSIDE

Back 130

mechanism: an analog of deoxyadenosine, phosphorylated by host cell enzymes to make adenine arbinoside triphosphate, incorporated into viral DNA by viral DNA polymerase, blocks further DNA synthesis (CHAIN TERMINATING ANALOGUE)

useful in HERPEs SIMPLEX ENCEPHALITIS and in some immunosuppressed patients with ZOSTER

largely supplanted by acyclovir

Front 131

FOSCARNET

Back 131

treats: (alternative to ganciclovir) for CMV infections

mechanism: analog of pyrophosphate
inhibitor of herpes DNA polymerase, has much less effect on DNA of human cells

Front 132

AEROSOLIZED RIBAVIRIN

Back 132

used to treat RSV pneumonia in infants

(efficacy uncertain)

Front 133

ALPHA INTERFERON (for months)

Alpha interveron + Ribavirin

Back 133

drug used to treat chronic hepatitis caused by HCV

Front 134

ALPHA INTERFERON LAMUVINDINE

Back 134

used to treat chronic heptatitis caused by HBV

Front 135

AMANTIDINE [RIMANTIDINE]

Back 135

used to treat INFLUENZA A (only A)

Front 136

OSELTAMIVIR [zanamivir]

Back 136

used to treat all influenza (A, B and C)

Front 137

ACYCLOVIR

Back 137

used to treat all severe primary infections with herpes simplex virus

also used prophlactically to reduce the incidence of recurrent herpes simplex infection, espeically genital and corneal (keratitis) lesions

Front 138

TRIFLURIDINE or ACYCLOVIR

Back 138

used to treat recurrent herpes simplex keratitis (non retinitis- note the anatomical difference)

Front 139

all severe varicella-zoster virus infections can be treated with

Back 139

acyclovir

Front 140

all severe CMV infecetions (mostly in immunosuppressed patients) can be treated with

Back 140

ganciclovir or goscarnet

Front 141

acyclovir-resisitant herpes simple or varicella-zoster virus infections can be treated with

Back 141

foscarnet