Download Viral Infections: an overview

Viral Infections: an overview
Dr. Meg-angela Christi Amores
Defining a Virus
• Viruses consist of a nucleic acid surrounded by
one or more proteins
• obligate intracellular parasites: they can
replicate only within cells
• Many human viruses are simply composed of
a core and a capsid
• Genes: contain either DNA or RNA
RNA Viruses
DNA Viruses
Picornaviruses
Poliovirus
Coxsackievirus
Echovirus
Enterovirus
Rhinovirus
Hepatitis A virus
Herpesviridae
Herpes simplex virus types 1 and 2b
Varicella-zoster virusc
Epstein-Barr virusd
Cytomegaloviruse
Human herpesvirus 6
Human herpesvirus 7
Calciviridae
Norwalk agent
Hepatitis E virus
Hepadnaviridae
Hepatitis B virus
Togaviridae
Rubella virus
Eastern equine encephalitis virus
Western equine encephalitis virus
Papovaviridae
Human papillomaviruses
JC virus
BK virus
Flaviviridae
Yellow fever virus
Dengue virus
St. Louis encephalitis virus
West Nile virus
Hepatitis C virus
Hepatitis G virus
Poxviridae
Variola (smallpox) virus
Orf virus
Molluscum contagiosum virus
RNA Viruses
DNA Viruses
Coronaviridae
Coronaviruses
Adenoviridae
Human adenoviruses
Rhabdoviridae
Rabies virus
Vesicular stomatitis virus
Parvoviridae
Parvovirus B19
Filoviridae
Marburg virus
Ebola virus
Paramyxoviridae
Parainfluenza virus
Respiratory syncytial virus
Newcastle disease virus
Mumps virus
Rubeola (measles) virus
Orthomyxoviridae
Influenza A, B, and C viruses
Bunyaviridae
Hantavirus
California encephalitis virus
Sandfly fever virus
• Transmission
Viral Infection
– capsid and envelope of a virus protect its genome
– Most common viral infections are spread by
• direct contact
• by ingestion of contaminated water or food
• by inhalation of aerosolized particles
– Animals are important reservoirs and vectors for
transmission of viruses causing human disease
Viral Infection
• Primary Infection
– usually lasts from several days to several weeks
• enterovirus, mumps virus, measles virus, rubella virus,
rotavirus, influenza virus, AAV, adenovirus, HSV, and
VZV are cleared from almost all sites within 3–4 weeks
• AAV, EBV, or cytomegalovirus (CMV) can last for several
months
• HBV, HCV, hepatitis D virus (HDV), HIV, HPV, and
molluscum contagiosum virus extend beyond several
weeks
Viral Infection
• Primary Infection
– Disease manifestations usually arise as a
consequence of viral replication and the resultant
inflammatory response
– are cleared by nonspecific innate and specific
adaptive immune responses
– host is usually immune to the disease
manifestations of reinfection by the same virus
Persistent and Latent Infections
– HCV RNA polymerase and HIV reverse
transcriptase have high mutation rates
– generation of variant genomes that evade the
host immune response facilitates persistent
infection
– DNA viruses: lower mutation rates
• ability to establish latent infection and to reactivate
from latency
Persistent and Latent Infections
• latency is defined as a state of infection in
which the virus is not replicating
• HPVs establish latent infection in basal
epithelial cells
Persistent and Latent Infections
• Herpesviruses: latent infection is established
– in nonreplicating neural cells (HSV and VZV)
– in replicating cells of hematopoietic lineages [EBV
and probably CMV, HHV-6, HHV-7, and Kaposi's
sarcoma–associated herpesvirus (KSHV, also
known as HHV-8)].
Persistent Viral infections and Cancer
– estimated to be the root cause of as many as 20%
of human malignancies
– Most hepatocellular carcinoma is now believed to
be caused by chronic inflammatory, immune, and
regenerative responses to HBV or HCV infection
– Almost all cervical carcinoma is caused by
persistent infection with "high-risk" genital HPV
strains
– EBV infection also plays a role in the long-term
development of certain B lymphocyte and
epithelial cell malignancies
Resistance to Viral Infections
• Initial response is not virus-specific
• Physical
– cornified layers of the skin and by mucous
secretions that continuously sweep over mucosal
surfaces
• Cellular
– IFNs are induced and confer resistance
– cytokines may be chemotactic to inflammatory
and immune cells
Resistance to Viral Infections
• By 7–10 days after infection, virus-specific
antibody responses develop
• virus-specific HLA class II–restricted CD4+ helper T
lymphocyte responses, and virus-specific HLA class I–
restricted CD8+ cytotoxic T lymphocyte responses
• Antibody and complement can also lyse virus-infected
cells that express viral proteins on their surface
• host inflammatory and immune response
contributes to the symptoms, signs, and other
pathophysiologic manifestations of viral
infection
Diagnostic Virology
• Serology
• Viral Isolation
• Acute- and convalescent-phase sera with
rising titers of antibody to virus-specific
antigens
• shift from IgM to IgG antibodies
Diagnostic Virology
• ELISA (Enyme-Linked Immunosorbent Assay)
– generally use specific viral proteins that are most
frequently targeted by the antibody response
– amount of antibody can then be quantitated by
the intensity of a color reaction mediated by the
linked enzyme
• Virus isolation
– depends on the collection of specimens from the
appropriate site
– the rapid transport of these specimens in the
appropriate medium to the virology laboratory
– Rapid transport maintains viral viability and limits
bacterial and fungal overgrowth.
Treatment
• Multiple steps in the viral life cycle can be
effectively targeted by antiviral drugs
– synthesis of the HIV provirus
– block maturation of the HIV polyprotein
– preventing a conformational change required for
virus fusion
– preventing release of viral RNA early during
infection
– Prevent efficient release of mature virions
Immunization
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Smallpox
Poliovirus
Measles
Influenza
Chickenpox
HBV
Mumps, rubella