PATHOGENESIS OF VIRAL INFECTIONS IN THE SKIN
There are three general patterns of viral infection
1- Acute infection followed by viral clearance, usually by immune mechanisms.
• This pattern occurs frequently with viruses that produce exanthemas, such as measles.
2- Acute infection followed by latent infection, which may then be followed by viral reactivation.
• In viruses with cutaneous manifestations, this pattern occur - HSV ,
- varicella-zoster virus (VZV) , - and papillomavirus.
3- chronic infection, as occurs with HIV.
Active subacute or chronic infections lasting months to years can also occur with papillomaviruses and MCV, even in immunocompetent hosts.
Transmission :
- shedding from human skin lesions in :
warts, herpes simplex, chickenpox, herpes zoster, mollu
- For other viruses with cutaneous manifestations, respiratory secretions, blood, genital secretions, or animal vectors are involved in carrying virus to susceptible individuals.
Skin affection :
The skin, specifically, is affected by three different routes:
The skin lesions that result may be produced by
1- Direct inoculation :
The viruses of warts, molluscum contagiosum, and
- All infect the skin by direct inoculation, replicate in the epidermis.
- The immune system presumably contributes to the evolution of these lesions by inducing an inflammatory response.
- The incubation period is generally short, b
For warts, however, the incubation period is longer, presumably because the virus replicates slowly or cell spread of virus occurs to only a limited extent.
2- In systemic infections :
- In systemic infections, the skin is infected during viremia, so that the dermis is generally infected earlier than the epidermis.
3- local spread from an internal focus :
- Recurrent herpes simplex and herpes zoster represent the local spread of virus to the reactivation of the latent virus present in sensory nerve ganglia.
PATHOGENESIS OF VIRAL INFECTIONS IN THE SKIN
There are three general patterns of viral infection :
cute infection followed by viral clearance, usually by immune mechanisms. (most typical This pattern occurs frequently with viruses that produce exanthemas, such as measles.
cute infection followed by latent infection, which may then be followed by viral reactivation.
In viruses with cutaneous manifestations, this pattern occurs often with:
chronic infection, as occurs with HIV.
Active subacute or chronic infections lasting months to years can also occur with papillomaviruses and MCV, even in
in :
warts, herpes simplex, chickenpox, herpes zoster, molluscum contagiosum, and smallpox.
For other viruses with cutaneous manifestations, respiratory secretions, blood, genital secretions, or animal ors are involved in carrying virus to susceptible individuals.
The skin, specifically, is affected by three different routes:
1- direct inoculation, 2- systemic infection, or
3- local spread from an internal focus.
that result may be produced by :
1- the direct effect of virus replication on infected cells, 2- the host response to the virus, or
3- the interaction of replication and host response.
The viruses of warts, molluscum contagiosum, and (primary) herpes simplex : direct inoculation, replicate in the epidermis.
The immune system presumably contributes to the evolution of these lesions by inducing an inflammatory The incubation period is generally short, because the lesions develop at the site of inoculation.
For warts, however, the incubation period is longer, presumably because the virus replicates slowly or cell spread of virus occurs to only a limited extent.
In systemic infections, the skin is infected during viremia, so that the dermis is generally infected earlier
spread from an internal focus :
Recurrent herpes simplex and herpes zoster represent the local spread of virus to the reactivation of the latent virus present in sensory nerve ganglia.
PATHOGENESIS OF VIRAL INFECTIONS IN THE SKIN
most typical pattern) This pattern occurs frequently with viruses that produce exanthemas, such as measles.
cute infection followed by latent infection, which may then be followed by viral reactivation.
Active subacute or chronic infections lasting months to years can also occur with papillomaviruses and MCV, even in
scum contagiosum, and smallpox.
For other viruses with cutaneous manifestations, respiratory secretions, blood, genital secretions, or animal
local spread from an internal focus.
the direct effect of virus replication on infected cells, the interaction of replication and host response.
The immune system presumably contributes to the evolution of these lesions by inducing an inflammatory ecause the lesions develop at the site of inoculation.
For warts, however, the incubation period is longer, presumably because the virus replicates slowly or cell-to-cell
In systemic infections, the skin is infected during viremia, so that the dermis is generally infected earlier
Recurrent herpes simplex and herpes zoster represent the local spread of virus to the skin after
HOST RESPONSE
The severity of illness induced by a particular virus varies 1- size of the viral inoculum and
2- the portal of entry play
3- immunologic and nonimmunologic responses appear to be important, key roles in the coordinated immune response.
Antibody responses to viral infection represent the major host defense against re There are several mechanisms by which antibodies m
1- neutralization of virus through prevention of viral attachment to target cells (which may be increased by complement),
2- enhancement of viral uptake by phagocytic cells, 3- complement-mediated immune lysis of infected cells.
However, humoral immunity is thought not to contribute to the recovery from most primary viral infections, Specific cell-mediated immunity (CMI) is also elicited during v
infections.
- CMI controls viral spread and promotes clearance of the virus, although it may sometimes increase the degree of cellular pathology (as in the eruption of measles).
- Patients with impaired CMI often have difficulty handling primary or recurrent viral infection.
- Such patients are at risk of developing severe primary virus infections, problematic reactivations of dormant viruses such as VZV and cytomegalovirus, and pers
lesions.
- Virus-specific cytotoxic lymphocytes, natural killer cells, and antibody inhibit infection under experimental conditions, and these are infections.
- Inflammatory cells may produce some of their antiviral effects via the production of closely related cytokines that are active against viruses.
• Interferon, which can be induced by foreign RNA or DNA (including viral nucleic acids), is secreted into the extracellular fluid. Resistance to viral infection is induced in those cells that come in contact with the interferon.
• Virtually all viruses are capable of
greatly in their degree of interferon induction and in their sensitivity to its effects.
• Genetic factors may also play a role in determining the outcome of viral infections. In anim
genes can determine the susceptibility to viral infection at several levels, including virion attachment to cells, viral replication, and viral-induced immune responses.
The severity of illness induced by a particular virus varies from person to person :
immunologic and nonimmunologic responses appear to be important,and both innate and adaptive immunity play key roles in the coordinated immune response.18
represent the major host defense against re-infection by the There are several mechanisms by which antibodies may inhibit the spread of virus, These include
neutralization of virus through prevention of viral attachment to target cells (which may be increased by ake by phagocytic cells, and
mediated immune lysis of infected cells.
However, humoral immunity is thought not to contribute to the recovery from most primary viral infections, is also elicited during viral infections and influences the course of many viral CMI controls viral spread and promotes clearance of the virus, although it may sometimes increase the degree of cellular pathology (as in the eruption of measles).
Patients with impaired CMI often have difficulty handling primary or recurrent viral infection.
Such patients are at risk of developing severe primary virus infections, problematic reactivations of dormant viruses such as VZV and cytomegalovirus, and persistent warts, herpes simplex eruptions, and other viral cutaneous
specific cytotoxic lymphocytes, natural killer cells, and antibody-dependent cell-mediated cytotoxicity all can inhibit infection under experimental conditions, and these are thought to be the primary players in clearing viral
Inflammatory cells may produce some of their antiviral effects via the production of interferons closely related cytokines that are active against viruses.20
, which can be induced by foreign RNA or DNA (including viral nucleic acids), is secreted into the extracellular fluid. Resistance to viral infection is induced in those cells that come in contact with the Virtually all viruses are capable of inducing interferon and are susceptible to its action, but viruses differ greatly in their degree of interferon induction and in their sensitivity to its effects.
Genetic factors may also play a role in determining the outcome of viral infections. In anim
genes can determine the susceptibility to viral infection at several levels, including virion attachment to cells, induced immune responses.21
and both innate and adaptive immunity play
infection by the same virus.
These include:
neutralization of virus through prevention of viral attachment to target cells (which may be increased by
However, humoral immunity is thought not to contribute to the recovery from most primary viral infections, iral infections and influences the course of many viral CMI controls viral spread and promotes clearance of the virus, although it may sometimes increase the degree of Patients with impaired CMI often have difficulty handling primary or recurrent viral infection.
Such patients are at risk of developing severe primary virus infections, problematic reactivations of dormant viruses istent warts, herpes simplex eruptions, and other viral cutaneous
mediated cytotoxicity all can thought to be the primary players in clearing viral
interferons, a unique family of
, which can be induced by foreign RNA or DNA (including viral nucleic acids), is secreted into the extracellular fluid. Resistance to viral infection is induced in those cells that come in contact with the
inducing interferon and are susceptible to its action, but viruses differ greatly in their degree of interferon induction and in their sensitivity to its effects.
Genetic factors may also play a role in determining the outcome of viral infections. In animal models, cellular genes can determine the susceptibility to viral infection at several levels, including virion attachment to cells,
