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Diagnosis of all other herpesvirus infection relies on isolation of the virus through As with herpes simplex virus, interferon and cellular and humoral immunity are and parenthetically provide unique sites for inhibition by antiviral agents.
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Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo , a bacterial infection. Common mouth ulcers aphthous ulcer also resemble intraoral herpes, but do not present a vesicular stage.

Genital herpes can be more difficult to diagnose than oral herpes, since most HSVinfected persons have no classical symptoms. Laboratory tests include culture of the virus, direct fluorescent antibody DFA studies to detect virus, skin biopsy , and polymerase chain reaction to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice. Until the s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.

It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster , which is caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin. As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.

Condom use also reduces the transmission risk significantly. However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.

Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore, if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir , in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.

To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSVseropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth e. Acyclovir is the recommended antiviral for herpes suppressive therapy during the last months of pregnancy.

The use of valaciclovir and famciclovir, while potentially improving compliance, have less-well-determined safety in pregnancy. No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol acetaminophen can reduce pain and fever. Topical anesthetic treatments such as prilocaine , lidocaine , benzocaine , or tetracaine can also relieve itching and pain. Several antiviral drugs are effective for treating herpes, including acyclovir , valaciclovir valacyclovir , famciclovir , and penciclovir.

Acyclovir was the first discovered and is now available in generic. Evidence supports the use of acyclovir and valacyclovir in the treatment of herpes labialis [59] as well as herpes infections in people with cancer. A number of topical antivirals are effective for herpes labialis, including acyclovir, penciclovir, and docosanol. Evidence is insufficient to support use of many of these compounds, including echinacea , eleuthero , L-lysine , zinc , monolaurin bee products, and aloe vera.

Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.

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Many HSV-infected people experience recurrence within the first year of infection. Prodromal symptoms include tingling paresthesia , itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster within 5—10 days without antiviral treatment than those occurring during the primary infection.

The causes of reactivation are uncertain, but several potential triggers have been documented. A study showed the protein VP16 plays a key role in reactivation of the dormant virus. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.

Other identified triggers include local injury to the face, lips, eyes, or mouth; trauma; surgery; radiotherapy ; and exposure to wind, ultraviolet light , or sunlight. The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days.

Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks.

An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes.

Antiviral medication has been proven to shorten the frequency and duration of outbreaks. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSVinfected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions. As many as one in seven Canadians aged 14 to 59 may be infected with herpes simplex type 2 virus [80] and more than 90 per cent of them may be unaware of their status, a new study suggests.

Herpes has been known for at least 2, years. Emperor Tiberius is said to have banned kissing in Rome for a time due to so many people having cold sores. In the 16th-century Romeo and Juliet , blisters "o'er ladies' lips" are mentioned. In the 18th century, it was so common among prostitutes that it was called "a vocational disease of women". Herpes was not found to be a virus until the s. Herpes antiviral therapy began in the early s with the experimental use of medications that interfered with viral replication called deoxyribonucleic acid DNA inhibitors. The original use was against normally fatal or debilitating illnesses such as adult encephalitis, [87] keratitis, [88] in immunocompromised transplant patients, [89] or disseminated herpes zoster.

The usage expanded to include topical treatment of herpes simplex, [92] zoster, and varicella. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U. Food and Drug Administration in Other experimental antivirals of that period included: Genital herpes simplex was not always stigmatised. It was merely a cold sore in an unusual place until the s. As late as , a study of "Psychological morbidity in a clinic for sexually transmitted disease" does not mention herpes simplex because at that time, no significant morbidity problem i.

Most had hardly heard of genital herpes Since the creation of the herpes hype, some people experience negative feelings related to the condition following diagnosis, in particular if they have acquired the genital form of the disease. Feelings can include depression , fear of rejection, feelings of isolation , fear of being found out, and self-destructive feelings. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late s and peaking in the early s.

Multiple articles were worded in fear-mongering and anxiety-provoking terminology, such as the now-ubiquitous "attacks", "outbreaks", "victims", and "sufferers". At one point, the term "herpetic" even entered the popular lexicon. The articles were published by Reader's Digest , U.

News , and Time magazine, among others. A made-for-TV movie was named Intimate Agony. The peak was when Time magazine had 'Herpes: The New Scarlet Letter' on the cover in August , forever stigmatizing the word in the public mind. People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.

One of the diseases that increased dramatically was genital herpes. Human herpesvirus 8 can be transmitted through exposure to infectious blood products. Cases of HHV-8 seroconversion associated with blood transfusion, organ transplantation, and intravenous drug use have been reported, however, the latter may be indicative of other high-risk behaviors associated with drug use Pica and Volpi, Blood-borne transmission directly exposes immune cells circulating in the vascular system, such as mDC, to the virus much quicker than natural exposure through the oral or genital route.

Differences in primary sites of HHV-8 infection likely influence the host response to infection. How HHV-8 travels to and infects cells within secondary lymphoid tissue is not fully understood. The mucosal immune system, both oral and urogenital, is highly sensitized to the detection of and protection from foreign microbes. However, when an organism breaches this primary line of defense, resident immune cells detect the intrusion and produce pro-inflammatory cytokines.

This triggers APC migration into lymphatic vessels and trafficking to draining lymph nodes where the foreign antigen is presented to effector T and B cells Holmgren and Czerkinsky, Human herpesvirus 8 likely travels to draining lymphoid organs within DC and monocytes from the primary site of infection, where it can then interact with resident B and T cells.

Lytic HHV-8 infection of oral epithelium occurs in vitro Duus et al. Macrophages found in tissues and monocytes in peripheral blood travel to draining lymph nodes upon stimulation by foreign microbial antigens, and function in antigen presentation. Therefore, it can be hypothesized that HHV-8 infects the mucosal epithelium and uses proximal DC, and possibly monocytes and macrophages, to penetrate the lymphatic system.

Immature B cells are abundant in the germinal centers of lymph nodes where they interact with antigen presenting follicular DC fDC and follicular T helper cells, and mature during somatic hypermutation and clonal expansion Beltman et al. Extensive evidence indicates that peripheral blood B cells from healthy individuals support productive lytic HHV-8 infection in vitro when activated with CD40L and IL-4, whereas tonsillar B cells do so without requiring ex vivo activation Rappocciolo et al.

It is unclear whether each of these B cell subsets is directly infected or derived from infected precursors. Studies are needed to more directly assess the role of HHV-8 infection of B cells in endothelial cell transformation associated with KS. This systemic, B cell cytokine and chemokine milieu could be important in driving endothelial cell outgrowth in KS, and contribute to the development of HHV-8 associated malignancies.

However, it is still unclear whether various B cell lineage subsets are equally susceptible to HHV-8 lytic and latent infection, or if B cell subset precursors are infected and as a result driven into differentiation. Follicular DC make up a subset of DC with ontogeny distinct from mDC and pDC that reside in secondary lymphoid organs and specialize in antigen presentation King and Katz, as well as provide anti-apoptotic stimuli during activation of B cells Park and Choi, In addition, Gregory et al.

Latent viral infection of the monocyte cell line was associated with a dampened inflammatory and adaptive immune response, indicated by a decrease in proinflammatory cytokine production and monocyte co-stimulatory molecule expression associated with T cell activation. It has also been reported that HHV-8 can enter T lymphocytes from tonsils and result in an abortive infection Myoung and Ganem, This must be viewed however, with the fact that HHV-8 infection does not result in high-risk for disease in immunocompetent people. Despite the wide range of permissive and potentially susceptible host cells and substantial immune modulation associated with infection, most HHVassociated pathologies only occur when the immune response is compromised by HIV-1 co-infection or another secondary mechanism such as immunosuppression caused by anti-rejection drugs during organ transplantation and by older age.

Based on such epidemiological data, substandard T cell function and consequent ineffective control of virus lytic reactivation are a major basis for susceptibility to HHV-8 disease. Perhaps what is most puzzling is that the extensive array of lytic and latent gene products encoded by HHV-8 that mimic host immunoregulatory proteins as well as growth factors are insufficient to cause KS Mesri et al.

We Knowlton et al. It is therefore likely that the impact of HHV-8 infection of DC on T and B cell cytokine and chemokine production is important in this pathogenic process. In addition, multiple cell types associated with the dermal and epidermal layers in KS lesions support their role in productive HHV-8 infection.

DC quantity and functional quality are lowered or skewed in classic KS patients. The likelihood of KS development and time to progression after HHV-8 seroconversion varies based on history of previous infections, HIV-1 co-infection, and behavioral characteristics Armenian et al.

Therefore, there may be events interfering with the anti-HHV-8 T cell response that begin years prior to disease. T cell responses to HHV-8 antigens and the role of DC in these have yet to be compared longitudinally from infection to KS development, and may reveal important implications of immune suppression and KS. Similarly, DC functional abnormalities have been associated with several cancers including melanoma and chronic lymphocytic leukemia Enk et al. This suggests that in addition to reducing the function of DC, HHV-8 can inhibit the activation and differentiation of monocytes into DCs.

Immune System Behavior during Herpesvirus Infection in Childhood | OMICS International

Interestingly, these same fDC are thought to facilitate the increase of T cell infiltration into these secondary lymphoid organs El-Daly et al. This suggests that fDC serve as functional soldiers in the DC arm of defense. Briefly, the design and use of DC-based treatment and vaccines targeting multiple myeloma was heavily considered and thought to be promising in the late s.

HHV-8 infection was initially found in bone marrow DC of patients with multiple myeloma Rettig et al. However, evidence since has concluded that bone marrow-derived Mitterer et al. In fact, the absence of HHV-8 in DC of these patients increases the feasibility of an autologous, DC-based immunomodulatory therapy for multiple myeloma. However, such treatments have rarely been successful in clinical trials.

Human herpesvirus 8 encodes many cellular protein homologs, such as vIL-6 Neipel et al. In addition, HHV-8 infection of DC precursor monocytes has been directly correlated with an inhibition of maturation into iDC and a decrease in functional stimulation of lymphocytes Cirone et al. A dysfunction in immune stimulation of infected DC is supported by earlier studies revealing two HHV-8 encoded proteins, K3 and K5, with essential roles in down-regulating MHC class I molecules via endocytosis from the surface of infected cells Coscoy and Ganem, ; Ishido et al.

However, their impact on DC function is not clear and could be studied with RNA silencing technology. Despite an increased progression to disease following immune suppression, it is puzzling how otherwise healthy individuals remain capable of minimizing HHV-8 pathogenesis even with viral factors directly attempting to inhibit the function of DC and other immune cells. Addressing this enigma requires in depth studies of HHV-8 infection of naturally targeted cells including DC. Together these data suggest that DC-SIGN is positively regulated in response to extracellular pathogen-based immune responses and negatively regulated in response to intracellular pathogen-based responses such as viral infections.

This theoretically should help decrease the number of HHV-8 susceptible cells in the host. Alternatively, uninfected DC at sites of infection could recognize and engulf distressed, lytically infected cells, such as apoptotic B cells, macrophages, and endothelial cells Ueno et al.

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All together these sustained DC functions should contribute to minimizing HHV-8 pathogenesis and allowing otherwise healthy individuals to handle this chronic infection over a lifetime. The natural progression of HHV-8 infection of humans is not fully understood. However, it most commonly begins with entry though a mucosal surface, and likely spreads through the lymphatic system through which it accesses immune cells in mucosal associated lymphoid tissue and the circulatory system.

The expression of viral cytokines, vGPCR, and microRNA homologs suggests that this virus goes to a great extent to alter host cellular activities in favor of viral replication, disease, and survival. It is, therefore, an enigma how humans deal with chronic life-long HHV-8 infections with minimal morbidity unless otherwise immunocompromised.

It is likely that, as with most chronic viral infections, severe disease is not an endpoint goal of HHV-8 in healthy individuals. The virus likely hinders the pathogen detection and surveillance arm of the immune system sufficiently to remain hidden, possibly within B cells. Despite a non-robust lytic replication cycle in DC, abortive HHV-8 infection is associated with dysfunctional maturation and a dampened T helper-1 response and up-regulation of T helper-2 cytokine production, yet such responses are sufficient to limit pathogenesis.

The MHCs can also be targeted for destruction in the proteasome or lysosome. This prevents the natural killer cell response.

Helicobacter pylori Infection and Immunity Infectious Agents and Pathogenesis

Below are the distinct viruses in this family known to cause disease in humans. In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections:. In animal virology , the best known herpesviruses belong to the subfamily Alphaherpesvirinae.

Research on pseudorabies virus PrV , the causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unraveling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1 , the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis , is analyzed to elucidate molecular mechanisms of latency.

The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae. Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. From Wikipedia, the free encyclopedia. Herpesviridae Virus classification Group: Gammaherpesvirinae Lymphocryptovirus Macavirus Percavirus Rhadinovirus Herpesviridae is a large family of DNA viruses that cause diseases in animals, including humans. Gallid herpesvirus 1 Psittacid herpesvirus 1.

Anatid herpesvirus 1 Columbid herpesvirus 1 Gallid herpesvirus 2 Gallid herpesvirus 3 Meleagrid herpesvirus 1. Ateline herpesvirus 1 Bovine herpesvirus 2 Cercopithecine herpesvirus 2 Human herpesvirus 1 Human herpesvirus 2 Leporid herpesvirus 4 Macacine herpesvirus 1 Macropodid herpesvirus 1 Macropodid herpesvirus 2 Papiine herpesvirus 2 Saimiriine herpesvirus 1.

Bovine herpesvirus 1 Bovine herpesvirus 5 Bubaline herpesvirus 1 Canid herpesvirus 1 Caprine herpesvirus 1 Cercopithecine herpesvirus 9 Cervid herpesvirus 1 Cervid herpesvirus 2 Equid herpesvirus 1 Equid herpesvirus 3 Equid herpesvirus 4 Equid herpesvirus 8 Equid herpesvirus 9 Felid herpesvirus 1 Human herpesvirus 3 Phocid herpesvirus 1 Suid herpesvirus 1.

Aotine herpesvirus 1 Cebine herpesvirus 1 Cercopithecine herpesvirus 5 Human herpesvirus 5 Macacine herpesvirus 3 Panine herpesvirus 2 Papiine herpesvirus 3 Saimiriine herpesvirus 4. Murid herpesvirus 1 Murid herpesvirus 2 Murid herpesvirus 8. Human herpesvirus 7 Human herpesvirus 6A Human herpesvirus 6B. Caviid herpesvirus 2 Suid herpesvirus 2 Tupaiid herpesvirus 1. Callitrichine herpesvirus 3 Cercopithecine herpesvirus 14 Gorilline herpesvirus 1 Human herpesvirus 4 Macacine herpesvirus 4 Panine herpesvirus 1 Papiine herpesvirus 1 Pongine herpesvirus 2.

Alcelaphine herpesvirus 1 Alcelaphine herpesvirus 2 Bovine herpesvirus 6 Caprine herpesvirus 2 Hippotragine herpesvirus 1 Ovine herpesvirus 2 Suid herpesvirus 3 Suid herpesvirus 4 Suid herpesvirus 5. Equid herpesvirus 2 Equid herpesvirus 5 Mustelid herpesvirus 1. Ateline herpesvirus 2 Ateline herpesvirus 3 Bovine herpesvirus 4 Cricetid herpesvirus 2 Human herpesvirus 8 Macacine herpesvirus 5 Murid herpesvirus 4 Murid herpesvirus 7 Saimiriine herpesvirus 2. Equid herpesvirus 7 Phocid herpesvirus 2 Saguinine herpesvirus 1. Sherris Medical Microbiology 4th ed. Molecular and Cellular Biology.

Virology, Principles and Applications. Newcomb August 1, Insights from Structural Analysis". Current Opinion in Virology. Retrieved 15 June Cellular and Molecular Immunology.

Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis.

Baron S; et al. Baron's Medical Microbiology 4th ed. Univ of Texas Medical Branch. Medical Microbiology 5th ed. Potential for Zoonotic Disease". The Example of Testudinid Herpesvirus 3". Veterinary Virology 2nd ed. Diseases of the skin and appendages by morphology. Freckles lentigo melasma nevus melanoma. Aphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous-cell carcinoma.

Adenoviridae Papillomaviridae Papovaviridae obsolete Polyomaviridae genera: