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Herpes simplex virions, TEM

It is a large group of DNA viruses that cause predominantly latent infections in animals and humans. The most important for a person are:

herpes simplex virus type 1 and 2 (HSV 1, 2)
varicella zoster virus (VZV)
cytomegalovirus (CMV)
Epstein-Barr virus (EBV, HHV 4)
human herpes viruses (HHV 6, 7, 8)

Virion

The capsid is coated with a lipid membrane. The virus is about 100-180 nm in size and is highly sensitive to external conditions (mainly fatty solvents and oxidizing agents). There is a tegument (protein layer) between the cover and the capsid. The cover predetermines some properties - viruses are sensitive to acidic pH and drying, as well as to non-polar solvents and detergents. Thus, the infection is transmitted only by direct contact with the infected person. .

Herpes simplex virus type 1 (HSV 1)

Herpes Virus

Diseases

clinical manifestation:

gingivostomatitis with fever, local lymfadenopathy – in early childhood
tonzilitis
keratoconjunctivitis
meningoencefalitis – it can manifest itself throughout life, has a difficult course, high lethality and leaves severe consequences after healing.
herpes labialis – manifestation in adults

Complications of primary infection - Kaposi's variceliform eruption (Eczema herpeticatum; vesicular-pustular)

Herpes simplex virus typ 2 (HSV2)

Diseases

it most often affects the mucous membranes of the genital tract (glans penis, cervix, vagina), especially in puberty. Fever and blisters are characteristic.
the virus may be excreted by cervical secretion.
development of severe generalized disease in neonatal infection

Pathogenesis

Gate of entry: the mucous membranes most often of the oral cavity
Multiplication of the virus
Spread through neurons to the sensory part of the trigeminal ganglia (ggl. Gasseri), where it persists.
During immunosuppression, endogenous infection is activated and herpes (herpes) develops.
the gateway for HSV 2 is the mucosa of the genital tract and the site of persistence = nerve ganglia in the small pelvis

Diagnostics

virus isolation from saliva, blister, cerebrospinal fluid
PCR
serological test for antibodies – ELISA

Epidemiology

The source of the virus is the person who excretes the virus through saliva, cervical secretion (symptoms of the disease may not be present).

Varicella zoster virus (VZV)

Diseases

Clinically, the virus manifests as chickenpox. The course is usually light with a slightly elevated temperature. If primary infection occurs in adulthood, complications can occur. Reactivation of the endogenous virus manifests itself clinically as shingles.

Pathogenesis

entrance gate - respiratory tract
multiplication
hematogenous to the skin and mucous membranes, where they form blisters
persistence in the spinal ganglia of the intercostal nerves - when the immunity is weakened, it spreads anterogradely into the sensitive area of the given nerve and shingles is formed.

Diagnostics

PCR

ELISA

Cytomegalovirus

It infects 90% of the adult population.

HE CMV lungs1

Primary infection

Primary infection is usually mild or asymptomatic. It manifests as:

infectious mononucleosis syndrome,
febrile illness with lymphadenitis,
hepatitis (especially in infants),
severe congenital infections (microcephaly, blindness, hepatomegaly, purpura),
congenital or postnatal infection - usually asymptomatic,
rarely pneumonia, colitis, meningitis.

Reactivation in immunosuppressed manifests as:

febrile illness with lymphadenitis,
pneumonia,
septic disease,
colitis, oesophagitis,
retinitis (especially in HIV positive),
encephalitis.

Following a kidney transplant, virus infection can cause transplant rejection.

Pathogenesis

The gateway is the respiratory tract or upper gastrointestinal tract. Then there is multiplication and subsequent hematogenous spread. It is associated with atherosclerosis and restenosis after heart surgery. The virus persists in salivary gland cells, renal tubules and leukocytes. An infected individual occasionally excretes viruses through saliva, urine, cervical secretion, and breast milk.

Diagnostics

Cultivation

Cultivation is easy. CMV grows with a typical cytopathic effect in 5-25 days on human diploid cells. Identification can be accelerated by evidence of nuclear inclusions with a mononuclear antibody (24-48 hours). We can use urine, saliva, vaginal secretion, breast milk (difficult), leukocytes (difficult) for cultivation.

Quick diagnostics

Antigen detection and microscopy are insensitive. Nucleic acid detection (PCR) is used, it is fast and reliable. Most sample types can be used. It is also possible to perform quantitative determinations. PCR is more sensitive than cultivation.

Evidence of antibodies

IgG, IgM or IgA are determined. IgG are anamnestic, they are of little importance for the diagnosis of reactivation, it is possible to determine the avidity of IgG. Both IgM and IgA are important in acute infections and reactivations. Non-specific reactions are described. Serology is only an orientation method. Antibodies do not indicate immunity.

Therapy

Hyperimmune gamma globulin
Antiviral therapy: ganciclovir; foscarnet; special new antivirals (cidofovir).
Prophylaxis in high risk patients; aciclovir (not suitable for the treatment of advanced infection).

Prevention

Vaccine attempts have so far failed. There are epidemiological measures in organ recipients (CMV negative recipients should not receive organs from a CMV positive donor) - due to the high population density, this is difficult to follow.

Epstein-Barr virus (EBV)

Epstein Barr Virus virions EM 10.1371 journal.pbio.0030430.g001-L

The widespread virus, from 10 years of age, is infected almost the entire population A small proportion is clinically manifest. It has been linked to Burkitt's lymphoma in Africa and nasopharyngeal carcinoma in Asia.

Diseases

clinical manifestations such as angina pectoris with lymphadenitis, fever and hepatic impairment.
relativně dlouh rekonvalescence

Pathogenesis

entrance gate - respiratory tract
proliferation and persistence in B-cells
persistent presence of antibodies and immunity to reinfection.

Diagnostics

isolation is complicated and practically impossible.
serological diagnostics: evidence of non-specific antibodies (Paul-Bunnell reaction), evidence of specific antibodies - indirect immunoflourescence, ELISA

Epidemiology

Thee virus spreads by droplets and is widespread worldwide.

HHV-6 a HHV-7

Sixth disease - exanthema subitum

HHV-6 and HHV-7 belong to the family Herpesviridae. HHV-6 is divided into two subspecies - HHV-6A and HHV-6B. They are enveloped viruses that contain double-stranded DNA. The size of the virion is 120-150 nm. They replicate in the nucleus, mature in the cytoplasm. They are lymphotropic viruses similar to CMV, they persist in the body for life.

Diagnostics

Based on clinical signs;
serology - IgG and IgM antibodies by immunofluorescence or ELISA methods;
cultivation - demanding, on special lymphocyte soils;
PCR - from different tissues, the most sensitive method.

Manifestations of infection

Primary infection usually takes place in childhood, often without symptoms. HHV-6 causes one of the most well-known manifestations of these viruses - a minor febrile condition in infants and young children with either exanthema - exanthema subitum (sixth childhood disease) or without skin manifestations. The severity increases with the occurrence of febrile convulsions. HHV-7 also produces similar symptoms. The infection spreads through the air. After an incubation period of 5-12 days, a high temperature without catarrhal manifestations lasting about 3 days, which is typical for the disease, begins. At a time of temperature drop, a small rash is sown, which must be distinguished from toxoalergic rash (after antibiotics, which are often given).

Rare clinical manifestations are encephalitis, hepatitis, event. infectious mononucleosis syndrome.

In immunosuppressed (lymphoproliferative diseases, after transplantation ...) there is a possibility of reactivation of the infection.

HHV-6A is more neurotropic, often detectable in patients with inflammatory CNS (multiple sclerosis).

Therapy

Therapy is only asymptomatic.

HHV-8

Kaposis Sarcoma Lesions

HHV-8 (Human Herpesvirus 8), also known as KSHV (Kaposi sarcoma-associated herpesvirus), is a dsDNA virus of the Herpesviridae family.
Described in patients with immune defects (HIV).
In immunodeficiency, it causes Kaposi's sarcoma (mesenchymal malignant vascular tumor).
Other diseases caused by the virus include primarily exudative lymphoma (when malignant B-lymphoma develops) or Castleman's disease.
It also occurs in immunocompetent individuals, causing only latent infection.

Diagnostics of the current state only by PCR.
Serological diagnostics: IgG antibodies - anamnestic

Links

Literature

HORÁČEK, Jiří. Základy lékařské mikrobiologie. 1. vydání. Praha : Nakladatelství Karolinum, 2000. sv. 1. ISBN 80-246-0006-4.
BEDNÁŘ, Marek. Lékařská mikrobiologie. 1. vydání. Marvil, 1999.
ŽAMPACHOVÁ, Eva. Přednášky a materiály dr. Žampachové ke stažení [online]. [cit. 2012-04-20]. <http://mujweb.cz/zampach/motol/?redirected=1521314685>.

References

Dostál, V. et al.:Infektologie. Karolinum, Praha, 2004, str. 247
NRL pro HV. HHV8 (KHSV) [online]. [cit. 2012-01-26]. <http://www.szu.cz/uploads/documents/CeM/Herp_viry/HHV8.pdf>.

@@ Line 32: / Line 32: @@
 * development of severe generalized disease in neonatal infection
-=== Patogenesis ===
+=== Pathogenesis ===
 * Gate of entry: the mucous membranes most often of the oral cavity
@@ Line 55: / Line 55: @@
 Clinically, the virus manifests as chickenpox. The course is usually light with a slightly elevated temperature. If primary infection occurs in adulthood, complications can occur. Reactivation of the endogenous virus manifests itself clinically as shingles.
-=== Patogeneze ===
+=== Pathogenesis ===
 * entrance gate - respiratory tract
@@ Line 74: / Line 74: @@
 Primary infection is usually mild or asymptomatic. It manifests as:
-* syndrom infekční mononukleózy,
+* '''[[infectious mononucleosis syndrome]]''',
-* horečnaté onemocnění s lymfadenitidou,
+* febrile illness with lymphadenitis,
-* hepatitida (hlavně u kojenců),
+* hepatitis (especially in infants),
-* závažné vrozené infekce (mikrocefalie, slepota, hepatomegalie, purpura),
+* '''severe congenital infections''' (microcephaly, blindness, hepatomegaly, purpura),
-* vrozená nebo postnatální infekce – většinou bezpříznaková,
+* congenital or postnatal infection - usually asymptomatic,
-* vzácně pneumonie, kolitida, meningitida. Reaktivace u imunosuprimovaných se projevuje jako:
+* rarely pneumonia, colitis, [[meningitis]].
-horečnaté onemocnění s lymfadenitidou,
-pneumonie,
-septické onemocnění,
-kolitida, oesophagitis,
-retinitida (hlavně u HIV pozitivních),
-encefalitida.
-Po transplantaci ledviny může být infekce virem důvodem rejekce transplantátu.
-Patogeneze
+Reactivation in '''immunosuppressed''' manifests as:
-Bránou vstupu je respirační trakt nebo horní část trávicí trubice. Potom dochází k pomnožení a následnému hematogennímu rozsevu. Váže se k ateroskleróze a restenózám po operacích srdce. Virus perzistuje v buňkách slinné žlázy, ledvinných tubulech a v leukocytech. Infikovaný jedinec občas vylučuje viry slinami, močí, cervikálním sekretem a mateřským mlékem.
-Diagnostika
+* febrile illness with lymphadenitis,
-Kultivace
+* [[Pneumonia (pediatrics)|pneumonia]],
-Kultivace je jednoduchá. CMV roste s typickým cytopatickým efektem za 5–25 dní na lidských diploidních buňkách. Identifikaci je možné urychlit důkazem jaderných inkluzí mononukleální protilátkou (24-48 hodin). Na kultivaci můžeme použít moč, sliny, poševní sekret, mateřské mléko (obtížně), leukocyty (obtížně).
+* [[septic disease]],
+* colitis, oesophagitis,
+* retinitis (especially in HIV positive),
+* [[encephalitis]].
-Rychlá diagnostika
+Following a kidney transplant, virus infection can cause transplant rejection.
-Důkaz antigenu a mikroskopie jsou málo citlivé. Používá se důkaz nukleové kyseliny (PCR). Ten je rychlý a spolehlivý. Možné použít většinu typů vzorků. Je možné provádět také kvantitativní stanovení. PCR je citlivější než kultivace.
-Důkaz protilátek
+=== Pathogenesis ===
-Stanovuje se IgG, IgM, případně IgA. IgG jsou anamnestické, pro diagnostiku reaktivace mají malý význam, možné stanovit aviditu IgG. IgM i IgA jsou důležité u akutních infekcí a reaktivací. Jsou popisované nespecifické reakce. Sérologie je pouze orientační metodou. Protilátky neznačí imunitu.
+The gateway is the respiratory tract or upper gastrointestinal tract. Then there is multiplication and subsequent hematogenous spread. It is associated with atherosclerosis and restenosis after heart surgery. The virus persists in salivary gland cells, renal tubules and leukocytes. An infected individual occasionally excretes viruses through saliva, urine, cervical secretion, and breast milk.
+=== Diagnostics ===
+==== Cultivation ====
+[[Cultivation]] is easy. CMV grows with a typical cytopathic effect in 5-25 days on human diploid cells. Identification can be accelerated by evidence of nuclear inclusions with a mononuclear antibody (24-48 hours). We can use urine, saliva, vaginal secretion, breast milk (difficult), leukocytes (difficult) for cultivation.
+==== Quick diagnostics ====
+Antigen detection and microscopy are insensitive. Nucleic acid detection (PCR) is used, it is fast and reliable. Most sample types can be used. It is also possible to perform quantitative determinations. PCR is more sensitive than cultivation.
+==== Evidence of antibodies ====
+IgG, IgM or IgA are determined. IgG are anamnestic, they are of little importance for the diagnosis of reactivation, it is possible to determine the avidity of IgG. Both IgM and IgA are important in acute infections and reactivations. Non-specific reactions are described. Serology is only an orientation method. Antibodies do not indicate immunity.
+=== Therapy ===
+* Hyperimmune gamma globulin
+* [[Antiviral therapy:]] ganciclovir; foscarnet; special new antivirals (cidofovir).
+* Prophylaxis in high risk patients; aciclovir (not suitable for the treatment of advanced infection).
+=== Prevention ===
+Vaccine attempts have so far failed. There are epidemiological measures in organ recipients (CMV negative recipients should not receive organs from a CMV positive donor) - due to the high population density, this is difficult to follow.
+== Epstein-Barr virus ([[EBV]]) ==
+[[File:Epstein Barr Virus virions EM 10.1371 journal.pbio.0030430.g001-L.JPG|thumb|Epstein Barr Virus virions EM 10.1371 journal.pbio.0030430.g001-L]]The widespread virus, from 10 years of age, is infected almost the entire population A small proportion is clinically manifest. It has been linked to Burkitt's lymphoma in Africa and nasopharyngeal carcinoma in Asia.
+=== Diseases ===
+* clinical manifestations such as angina pectoris with lymphadenitis, fever and hepatic impairment.
+* relativně dlouh rekonvalescence
+=== Pathogenesis ===
+* entrance gate - respiratory tract
+* proliferation and persistence in B-cells
+* persistent presence of antibodies and immunity to reinfection.
+=== Diagnostics ===
+* isolation is complicated and practically impossible.
+* '''serological diagnostics''': evidence of non-specific antibodies (Paul-Bunnell reaction), evidence of specific antibodies - indirect immunoflourescence, ELISA
+=== Epidemiology ===
+Thee virus spreads by droplets and is widespread worldwide.
+== HHV-6 a HHV-7 ==
+[[File:Sestamalattia (2).JPG|thumb|Sixth disease - exanthema subitum]]HHV-6 and HHV-7 belong to the family Herpesviridae. HHV-6 is divided into two subspecies - HHV-6A and HHV-6B. They are '''enveloped viruses''' that contain '''double-stranded DNA'''. The size of the virion is 120-150 nm. They replicate in the nucleus, mature in the cytoplasm. They are lymphotropic viruses similar to CMV, they persist in the body for life.
+=== Diagnostics ===
+* Based on clinical signs;
+* serology - IgG and IgM antibodies by immunofluorescence or ELISA methods;
+* cultivation - demanding, on special lymphocyte soils;
+* PCR - from different tissues, the most sensitive method.
+=== Manifestations of infection ===
+Primary infection usually takes place in childhood, often without symptoms. '''HHV-6''' causes one of the most well-known manifestations of these viruses - a minor '''febrile condition in infants and young children''' with either exanthema - '''exanthema subitum''' (sixth childhood disease) or without skin manifestations. The severity increases with the occurrence of '''[[febrile convulsions]]'''. '''HHV-7''' also produces similar symptoms. The infection spreads through the air. After an incubation period of 5-12 days, a high temperature ''without catarrhal manifestations'' lasting about 3 days, which is typical for the disease, begins. At a time of temperature drop, a small rash is sown, which must be distinguished from toxoalergic rash (after antibiotics, which are often given).
-Terapie
-Hyperimunní gamaglobulin
-Antivirová léčba:
-ganciklovir;
-foscarnet;
-speciální nová antivirotika (cidofovir).
-Profylaxe u pacientů s vysokým rizikem;
-aciklovir (není vhodný pro léčbu rozvinuté infekce).
-Prevence
-Pokusy o vakcínu jsou zatím neuspěšné. Existují epidemiologické opatření u příjemců orgánů (CMV negativní příjemce by neměl dostat orgány od CMV pozitivního dárce) – vzhledem k vysoké promořřenosti populace se to obtížně dodržuje.
-Epstein-Barrové vírus (EBV)
+Rare clinical manifestations are '''[[encephalitis]]''', '''hepatitis''', event. '''[[infectious mononucleosis syndrome]]'''.
-Searchtool right.svg Podrobnější informace naleznete na stránce EBV.
-Virion EBV
+In immunosuppressed (lymphoproliferative diseases, after transplantation ...) there is a possibility of reactivation of the infection.
-Rozšířený virus, od 10 roků života je promořená prakticky celá . Malá část se klinicky manifestuje. Byla zjištěna souvislost s Burkittovým lymfomem dětí v Africe a nazofaryngeálním karcinomem v Ázii.
-Onemocnění
+HHV-6A is more neurotropic, often detectable in patients with inflammatory CNS (multiple sclerosis).
-klinický projev jako povlaková angína s lymfadenitidou, horečkou a poruchou funkce jater.
-relativně dlouhá rekonvalescence
-Patogeneze
-brána vstupu – respirační trakt
-pomnožení v B – lymfocytech a perzistence
-trvalá přítomnost protilátek a imunita vůči reinfekci.
-Diagnostika
-izolace je složitá a prakticky se nedělá.
-sérologická diagnostika
-důkaz nespecifických protilátek (Paul-Bunnellova reakce,...)
-důkaz specifických protilátek – nepřímá imunoflourescence, ELISA
-Epidemiologie
-Virus se šíří kapénkami a je celosvětově rozšířený.
-HHV-6 a HHV-7
+=== Therapy ===
-[ ✎ upravit vložený článek ]
+Therapy is only asymptomatic.
-Šestá dětská nemoc.
+== HHV-8 ==
-HHV-6 a HHV-7 patří do čeledi Herpesviridae. HHV-6 se dělí na dva poddruhy – HHV-6A a HHV-6B. Jsou to obalené viry, které obsahují dvouvláknovou DNA. Velikost virionu je 120–150 nm. Replikují se v jádře, dozrávají v cytoplazmě. Jsou to lymfotropní viry podobné CMV, v organizmu perzistují celoživotně.
+[[File:Kaposis Sarcoma Lesions.jpg|thumb|Kaposis Sarcoma Lesions]]
-Diagnostika
+* HHV-8 (Human Herpesvirus 8), also known as KSHV (Kaposi sarcoma-associated herpesvirus), is a dsDNA virus of the Herpesviridae family.
-Na základě klinických příznaků;
+* Described in patients with immune defects (HIV).
-sérologie – protilátky IgG a IgM metodami imunofluorescence nebo ELISA;
+* In immunodeficiency, it causes Kaposi's sarcoma (mesenchymal malignant vascular tumor).
-kultivace – náročná, na speciálních lymfocytárních půdách;
+* Other diseases caused by the virus include primarily exudative lymphoma (when malignant B-lymphoma develops) or Castleman's disease.
-PCR – z různých tkání, nejcitlivější metoda.
+* It also occurs in immunocompetent individuals, causing only latent infection.
-Projevy infekce
-Primoinfekce obvykle probíhá v dětském věku, často probíhá bez příznaků. HHV-6 vyvolává jeden z nejznámějších projevů těchto virů − nezávažný febrilní stav u kojenců a malých dětí buď s exantémem – exanthema subitum (šestá dětská nemoc), anebo bez kožních projevů. Závažnost stoupá s výskytem febrilních křečí. Podobné projevy vyvolává také HHV-7. Infekce se šíří vzduchem. Po inkubační době 5-12 dní nastupuje vysoká teplota bez katarálních projevů trvající asi 3 dny, která je pro onemocnění typická. V době poklesu teploty dochází k výsevu drobného exantému, který je nutný odlišit od toxoalergického exantému (po antibiotikách, které jsou často podávané).
+* Diagnostics of the current state only by PCR.
+* Serological diagnostics: IgG antibodies - anamnestic
-HHV-6 v elektronovém mikroskopu
+== Links ==
-Vzácnejšími klinickými projevy jsou encefalitidy, hepatitidy, event. syndrom infekční mononukleózy.[1]
-U imunosuprimovaných (lymfoproliferativní onemocnění, po transplantaci...) je možnost reaktivace infekce.
+=== Related articles ===
-HHV-6A je víc neurotropní, často ho můžeme detekovat u pacientů se zanětlivým onemocněním CNS (sclerosis multiplex).
+* [[Herpetic encefalitis]]
+* [[Infection caused by HHV-6 and HHV-7]]
-Terapie
+=== Literature ===
-Terapie je symptomatická.
-HHV-8
+* HORÁČEK, Jiří. Základy lékařské mikrobiologie. 1. vydání. Praha : Nakladatelství Karolinum, 2000. sv. 1. ISBN 80-246-0006-4.
-[ ✎ upravit vložený článek ]
+* BEDNÁŘ, Marek. Lékařská mikrobiologie. 1. vydání. Marvil, 1999.
-Lidský herpetický virus 8
+* ŽAMPACHOVÁ, Eva. Přednášky a materiály dr. Žampachové ke stažení [online]. [cit. 2012-04-20]. <http://mujweb.cz/zampach/motol/?redirected=1521314685>.
-Herpesviridae
-Kaposiho sarkom
-Kaposiho sarkom
-Typ NK	dsDNA
-Zdroj	člověk
-Přenos	pohlavním stykem, krví
-Výskyt	kosmopolitní
-Onemocnění	Kaposiho sarkom (HIV+), jiné malignity (angiosarkom), Castlemanova choroba
-Diagnostika	sérologie, detekce protilátek proti jadernému antigenu, HHV-8 DNA
-Terapie	zatím neznáme účinnou kauzální léčbu
-MeSH ID	D019288
-HHV-8 (Human Herpesvirus 8), označovaný také jako KSHV (Kaposi sarcoma-associated herpesvirus), je dsDNA virus z čeledi Herpesviridae.
+=== References ===
-Popsán u pacientů s defektem imunity (HIV).
-U imunodeficientních způsobuje Kaposiho sarkom (mesenchymální maligní vaskulární nádor).
-Mezi další onemocnění způsobené virem se řadí primárně exsudativní lymfom (kdy vzniká maligní B-lymfom) nebo také Castlemanova choroba.
-Vyskytuje se i u imunokompetentních osob, u nich způsobuje jen latentní infekci.
-Diagnostika aktuálního stavu jen pomocí PCR.
-Sérologická diagnostika: IgG protilátky – anamnestické [2].
-Odkazy
-Související články
-Herpetická encefalitida
-Infekce vyvolané HHV-6 a HHV-7
-Použitá literatura
-HORÁČEK, Jiří. Základy lékařské mikrobiologie. 1. vydání. Praha : Nakladatelství Karolinum, 2000. sv. 1. ISBN 80-246-0006-4.
-BEDNÁŘ, Marek. Lékařská mikrobiologie. 1. vydání. Marvil, 1999.
-ŽAMPACHOVÁ, Eva. Přednášky a materiály dr. Žampachové ke stažení [online]. [cit. 2012-04-20]. <http://mujweb.cz/zampach/motol/?redirected=1521314685>.
-Reference
   Dostál, V. et al.:Infektologie. Karolinum, Praha, 2004, str. 247
   NRL pro HV. HHV8 (KHSV) [online]. [cit. 2012-01-26]. <http://www.szu.cz/uploads/documents/CeM/Herp_viry/HHV8.pdf>.