До питання про герпетичну інфекцію як актуальну проблему сьогодення

Relevance.There is no predominant agent in the etiological structure of hemorrhagic vasculitis; instead, several factors play a role, including the activation of herpesvirus infections in the disease development. The objective of the study is determined by contradictory data and a lack of coordinated agreement regarding the etiology of hemorrhagic vasculitis. Objective: To identify the role of herpesvirus infection in the etiology of hemorrhagic vasculitis in children. Materials and methods. A cross-sectional study was conducted for 25 children aged from 2 months to 18 years with hemorrhagic vasculitis, who were on inpatient treatment at Medical Center "Children's Hospital" in Aktobe. All children underwent an enzyme-linked immunosorbent assay (ELISA) for herpesviruses: herpes simplex virus types I, II, (HSV-I, II), Epstein - Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus type 6 (HHV – 6). The received data is processed by descriptive statistics, STATISTICS 10.0. Results The herpesvirus infection was confirmed in 100% of the examined children, with herpes simplex virus I and II types being discovered in 25.9% of cases, Epstein-Barr virus in 28.46% of cases, cytomegalovirus (CMV) in 29.6% of cases, and human herpesvirus 6 (HHV-6) in 16% of cases. Moreover, they did not occur as mono-infections but rather in conjunction with the cytomegalovirus: CMV+ HSV-I, II (16 %); CMV+ EBV (8%); CMV+ HHV-6 (4%); CMV+ EBV+ HHV-6 (32%); CMV+ HSV-I, II + EBV+ HHV-6 (40%). A low concentration of herpesvirus antibodies in the blood of patients with hemorrhagic vasculitis was detected by ELISA anti-CMV IgG (11.62 U / ml), anti-HHV-6 IgG (6.82 U/ml), which indicates unstable immunity, the risk of activation of viral infection and recurrent hemorrhagic vasculitis. Conclusion.According to the study, herpesvirus infections can lead to hemorrhagic vasculitis in children. If vasculitis recurs, it is advised to check for the presence of antibodies to herpesvirus antigens; if so, an infectious neurologist's consultation and etiotropic antiviral therapy are advised. Актуальность. В этиологической структуре геморрагического васкулита нет преобладания какого-либо одного агента, а играет роль совокупность нескольких факторов, в том числе активация герпесвирусных инфекций в развитии болезни. Противоречивые данные, отсутствие единого мнения об этиологии геморрагического васкулита определяет цель исследования. Цель. Определить роль герпесвирусной инфекции в этиологии геморрагического васкулита у детей. Материалы и методы. Одномоментное поперечное исследование проведено 25 детям с диагнозом геморрагический васкулит в возрасте от 2 мес. до 18 лет, которые находились на стационарном лечении в Актюбинском Медицинском Центре «Детском стационаре» г. Актобе. Всем детям проводился иммуноферментный анализ (ИФА) на герпесвирусы: вирус простого герпеса I, II-го типов, (HSV- I, II), вирус Эпштейна – Барр (EBV), цитомегаловирус (CMV), вирус герпеса человека 6-го типа (HHV-6). Полученные данные обработаны описательной статистикой, СТАТИСТИКА 10.0. Результаты. Герпесвирусная инфекция у обследуемых детей подтверждена в 100% случаев, из них вирус простого герпеса І, ІІ-го типов выявлен в 25,9%, вирус Эпштейна – Барр – 28,46%, цитомегаловирус (CMV) – 29,6%, вирус герпеса человека 6-го типа (HHV-6) – 16% случаев. И они не встречались как моноинфекции, а в виде ассоциации с цитомегаловирусом: CMV+ HSV-I, II (16 %); CMV+ EBV (8%); CMV+ HHV-6 (4%); CMV+ EBV+ HHV-6 (32%); CMV+ HSV-I, II + EBV+ HHV-6 (40 %). Выявлено малая концентрация антител герпесвирусов в крови больных с геморрагическим васкулитом методом ИФА анти-CMV IgG (11,62 ЕД/мл), анти-HHV-6 IgG (6,82 ЕД/мл), что свидетельствует о неустойчивом иммунитете, риске активации вирусной инфекции и рецидивирующим течением геморрагического васкулита. Заключение. Исследование показало роль герпесвирусной инфекций в развитии геморрагического васкулита у детей и при рецидивирующем васкулите рекомендуется обследование на наличие антител на антигены герпесвирусов и при их положительном результате рекомендуется консультация инфекциониста о решении этиотропной противовирусной терапии. Өзектілігі. Геморрагиялық васкулиттің этиологиялық құрылымында бір агент басым болмайды, бірақ бірнеше факторлардың жиынтығы, соның ішінде аурудың дамуындағы герпесвирустық инфекциялардың белсендірілуі маңызды рөл атарады. Қарама-қайшы дәлелдер, геморрагиялық васкулиттің этиологиясы туралы бірдей тұжырымның болмауы зерттеу мақсатын анықтайды. Мақсаты. Балалардағы геморрагиялық васкулиттің этиологиясындағы герпесвирустық инфекцияның рөлін анықтау. Материалдар мен әдістер. Ақтөбе қаласының Ақтөбе Медициналық орталығы Балалар стационарында" геморрагиялық васкулитпен стационарлық ем қабылдаған 2айдан 18 жасқа дейінгі 25 балаға бір мезгілде көлденең зерттеу жүргізілді. Барлық балаларға герпесвирустарға иммуноферменттік талдау (ИФА) жүргізілді: I, II типті қарапайым герпес вирусы, (HSV-I, II), Эпштейн - Барр вирусы (EBV), цитомегаловирус (CMV), 6 типті адамның герпес вирусы (HHV–6). Алынған мәліметтер сипаттамалық статистикамен өңделді, СТАТИСТИКА 10.0. Нәтижелері. Зерттелеген балалардағы герпесвирустық инфекция 100% жағдайда расталды, оның ішінде І, ІІ типті қарапайым герпес вирусы 25,9%, Эпштейн – Барр вирусы – 28,46%, цитомегаловирус (CMV) – 29,6%, 6 типті (HHV-6) адамның герпес вирусы -16% жағдайлар анықталды. Олар моноинфекция ретінде емес, цитомегаловируспен байланыс ретінде пайда болды: CMV+ HSV-I, II (16 %); CMV+ EBV (8%); CMV+ HHV-6 (4%); CMV+ EBV+ HHV-6 (32%); CMV+ HSV-I, II + EBV+ HHV-6 (40 %).Геморрагиялық васкулитпен ауыратын науқастардың қанында герпесвирус антиденелерінің төмен концентрациясы анти-CMV IgG (11,62 бірл/мл), анти-HHV-6 IgG (6,82 бірл/мл) ИФА әдісімен анықталды, бұл тұрақсыз иммунитетті, вирустық инфекцияны белсендіру қаупін және геморрагиялық васкулиттің қайталанатын ағымын көрсетеді. Қорытынды. Зерттеу балалардағы геморрагиялық васкулиттің дамуындағы герпесвирустық инфекциялардың рөлін көрсетті және қайталанатын васкулит кезінде герпесвирус антигендеріне антиденелердің болуын тексеру ұсынылады және олардың оң нәтижесі болған кезде этиотропты вирусқа қарсы терапияны шешу үшін инфекционистпен кеңес жүргізу ұсынылады.

Viral encephalitis.

A multiplex PCR assay was developed that enabled the simultaneous detection of DNA from 6 types of human herpes virus, HSV-1/2, VZV, EBV, CMV, HHV-6A/B, and HHV-7, using appropriate primer sets and conventional PCR techniques and instruments, with PCR products for each type of virus designed to be easily distinguishable by size. Electropherograms obtained from conventional agarose gels showed that, for each type, the observed number of base pairs corresponded to the intended product and that bands were easily distinguishable from each other. A minimum of 20 copies of viral DNA in a reaction was sufficient to confirm the existence of each of the 6 types of human herpes virus. Comparison of the data obtained from this method and the data obtained from conventional TaqMan PCR using clinical specimens from various sources showed consistent results. The multiplex PCR method reported here for the detection and differentiation of human herpes viruses did not require special equipment or techniques such as hybridization analysis and sequencing analysis and, therefore, enabled us to easily and rapidly detect and identify the 6 types of human herpes virus using conventional methods.

The study objective is to evaluate the prevalence of Epstein—Barr virus (EBV), herpes virus, human papillomavirus (HPV), and cytomegalovirus (CMV) infection among patients with cancer of the nasal cavity and paranasal sinuses in the Arkhangelsk Region.Materials and methods. We examined surgical specimens from 100 patients treated in the Arkhangelsk Clinical Oncology Dispensary between 2010 and 2015. Tissue homogenates were used for DNA isolation. DNA amplification with subsequent detection was performed using polymerase chain reaction.Results and conclusion. The 36 % of study participants were infected with EBV; the second most common viral pathogens were CMV and human herpes virus type 6 (HHV-6), both found in 21 % of cases. Monoinfection was observed in less than one-third of patients (20 % — EBV, HPV type 16 — 6 %), whereas the remaining participants had mixed infections: EBV + HHV-6 (2 %), CMV + EBV (5 %), EBV + herpes simplex virus types 1 and 2 (HSV-1,2) (1 %), EBV + CMV + HHV-6 (3 %), HPV type 16 + HSV-1,2 (3 %), and HPV type 6 + HPV type 16 (7 %). None of the patients with stage I cancer had mixed infections, whereas participants with stage II, III, and IV cancer demonstrated mixed infections in 1 %, 11 %, and 9 % of cases respectively.After specific treatment, 11 patients (30.5 %) infected with EBV developed regional metastases and 5 patients (13.9 %) had relapses. All patients simultaneously infected with EBV and HHV-6 had distant metastases. Combination of EBV, CMV, and HHV-6 resulted in relapses in 100 % of cases and distant metastasis in 75 % of cases.

Introduction. Currently, a role for human herpes viruses (HHV) in development of ocular oncopathology remains one of the poorly explored issues. An important factor contributing to neoplastic progression is impaired immunosurveillance particularly alterations in quantitative and qualitative composition of the hallmark peripheral blood lymphocyte subsets. The aim of the study was to determine and analyze peripheral blood lymphocyte subset composition in patients with uveal melanoma (UM) assessing human herpes viruses (HHV) infection in tumor material. Materials and methods. Biomaterial from 99 patients with uveal tract tumors was examined by real-time polymerase chain reaction (rt-PCR) for DNA presence coupled to herpes virus type 1 and 2 (HSV-1,2), Varicella Zoster virus (VZV), cytomegalovirus (CMV), Epstein–Barr virus (EBV), human herpes virus types 6 and 8 (HHV-6, HHV-8). A total of 231 test samples (tumor tissue (n = 99), blood (n = 132)) were examined. Commercial test-systems of “Vector-Best” (Russia) were used for rt-PCR staging. Peripheral blood lymphocyte subset composition in all patients was studied by laser cytofluorometry on “BD FACSCanto II” flow cytometer. The control group included 33 healthy donors. Statistical data processing was performed using “Biostatd”, “Excel” (t — Student’s t-test, level of statistical significance: p 0.05) software. Results. HHV DNA was detected in the tumor material from 11.3% of patients (n = 11): in 72.7% of cases EBV, in 18.2% — HHV-6. Co-infection with EBV and HHV-6 was detected in 1 case (retinal pigment epithelium adenocarcinoma). According to the PCR data, patients were divided into 2 groups based on tumor infectivity: Group 1 — HHV+ and Group 2 — HHV–. Patients from HHV+ group had significantly increased and decreased total T-cell (CD3+) and NK-cell count, respectively, compared with patients lacking HHV DNA in tumor tissue and control group. Individual analysis of frequencies deviating from normal range showed that HHV+ group had 3-fold more often increased percentage of CD3+ lymphocytes, 2-fold more often absolute count of CD3+CD4+CD8+ cells, 2.3-fold more often rise in CD4+/CD8+ ratio. Conclusion. The obtained data suggest that viruses may be involved in maintaining immunological resistance in tumor patients.

Human herpesvirus (HHV) infections are common during infancy. Primary infections are frequently asymptomatic and best studied prospectively by using direct viral detection. Oropharyngeal swab specimens were collected weekly from Ugandan newborn infants, their mothers, and other children in the household. Blood specimens were collected every 4 months. Samples were tested for herpes simplex virus (HSV) types 1 and 2, Epstein-Barr virus (EBV), cytomegalovirus (CMV), HHV-6A, HHV-6B, and HHV-8, using quantitative polymerase chain reaction. Thirty-two infants, 32 mothers, and 49 other household children were followed for a median of 57 weeks. Seventeen mothers had human immunodeficiency virus type 1 (HIV) infection; no infants acquired HIV-1. The 12-month incidence of postnatal infection was 76% for HHV-6B, 59% for CMV, 47% for EBV, 8% for HSV-1, and 0% for HHV-8. The quantity of oropharyngeal shedding by contacts was associated with HHV-6A or HHV-6B transmission. Maternal HIV-1 infection was associated with EBV transmission, while breastfeeding and younger child contacts were associated with CMV transmission. Except for HSV-1, primary HHV infections were subclinical. By capturing exposures and acquisition events, we found that the incidence and risk factors of infection vary by HHV type. HSV-1 infection, unlike other HHV infections, caused acute clinical illness in these infants.

Little is known about the prevalence and pathogenicity of human herpes viruses except for cytomegalovirus (CMV) in patients with inflammatory bowel disease (IBD). The aim of this study was to determine the prevalence of human herpes viruses on colonic mucosa in patients with IBD and assess the long-term outcomes in these patients. We examined the colonic mucosal specimens from 66 patients with ulcerative colitis (UC), 54 patients with Crohn's disease (CD), and 29 healthy patients to identify the 6 most common types of human herpes virus, using multiplex polymerase chain reaction (PCR) technique. Herpes simplex virus (HSV)-1/2 and varicella-zoster virus (VZV) were not detected in any of the groups. There was a higher prevalence of Epstein-Barr virus (EBV) (21.2%) and CMV (15.1%) in patients with UC than in patients with CD (EBV 9.3%, CMV 0%) and patents in the healthy control group (EBV 0%, CMV 3.4%). The prevalence of human herpes virus (HHV)-6A/B and HHV-7 was not statistically different among the groups. Five UC patients with inflammation had coexisting CMV and EBV or HHV-6. The combined infection of CMV with EBV or HHV-6 was a significant and independent prognostic factor for subsequent colectomy in patients with UC. The increased prevalence of CMV coexisting with EBV/HHV-6 infection was associated with the clinical course in patients with UC. 10.1093/ibd/izy005_video1izy005_Video_15786489376001.

Herpesviruses and the microbiome

Objective. To analyze circulation of herpes simplex virus (HSV), Epstein–Barr virus (EBV), cytomegalovirus (CMV), and human herpes virus type six (HHV-6) within families, to evaluate the conditions of formation of family foci, and to identify possible sources of infection. Patients and methods. We examined 124 families, including 11 two-parent families (mother, father, and child) and 108 oneparent families (mother and child). Five families had a mother and two children. Antibodies of various classes against herpesviruses were detected using enzyme-linked immunosorbent assay (ELISA). Herpesvirus antigens were detected using indirect immunofluorescence assay; early antigens and herpesvirus reproduction were evaluated using culture method; viral DNA was identified using polymerase chain reaction. Results. We have revealed a high rate of infection with herpesviruses in both adults and children. Markers of infections caused by HSV and EBV were detected in the majority of mothers (96.0% and 90.3%; 119 and 112), while children had these infections less frequently (66.7% in each group (86)). Detection of active forms of infection and convalescents, both among children and adults, indicates an intensive circulation of herpesviruses within families and leads to the formation of family foci of infection. Active infections were primarily caused by CMV (20.2% of children, 17.8% of mothers, and 15.4% of fathers) and EBV (16.3% of children, 11.3% of mothers, and 9.1% of fathers). Out of 266 participants examined (mothers, fathers, and children), cases of acute mixed infection were observed in children only (4 of 129) and were caused by HHV-6 in combination with HSV (2 cases) or CMV (2 cases). Conclusion. Continuous and intensive circulation of herpesviruses in families leads to the formation of family foci of infection. To stop intra-family transmission of viruses, it is important to identify possible sources of infection and perform antiepidemic measures. This transmission is most likely to occur in families where the mother has markers of active or recent infection, while the child does not have them at all. Such combination was detected in 16 patients with EBV (12.4%), 10 patients with HHV-6 (7.8%), 6 patients with HSV (4.7%), and 5 patients with CMV (3.9%). It is crucial to identify the role of the child as a source of herpesvirus infection. Key words: herpesvirus infections, infection markers, family foci, cytomegalovirus infection.

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.

In the battle to quickly identify potential yellow fever arbovirus outbreaks in the Democratic Republic of the Congo, active syndromic surveillance of acute febrile jaundice patients across the country is a powerful tool. However, patients who test negative for yellow fever virus infection are too often left without a diagnosis. By retroactively screening samples for other potential viral infections, we can both try to find sources of patient disease and gain information on how commonly they may occur and co-occur. Several human arboviruses have previously been identified, but there remain many other viral families that could be responsible for acute febrile jaundice. Here, we assessed the prevalence of human herpes viruses (HHVs) in these acute febrile jaundice disease samples. Total viral DNA was extracted from serum of 451 patients with acute febrile jaundice. We used real-time quantitative PCR to test all specimens for cytomegalovirus (CMV), herpes simplex virus (HSV), human herpes virus type 6 (HHV-6) and varicella-zoster virus (VZV). We found 21.3% had active HHV replication (13.1%, 2.4%, 6.2% and 2.4% were positive for CMV, HSV, HHV-6 and VZV, respectively), and that nearly half (45.8%) of these infections were characterized by co-infection either among HHVs or between HHVs and other viral infection, sometimes associated with acute febrile jaundice previously identified. Our results show that the role of HHV primary infection or reactivation in contributing to acute febrile jaundice disease identified through the yellow fever surveillance program should be routinely considered in diagnosing these patients.

Acute and chronic infections of the seminal tract are among the most common causes of male infertility. As at least half of male infertility cases are classified as idiopathic, some of these cases might be attributed to asymptomatic infection. The detection and quantification of Epstein-Barr virus (EBV), cytomegalovirus (CMV) and human herpes virus type 6 (HHV-6) DNA in semen samples were performed. A total of 232 patients were divided into five groups: (i) infertile men with varicocoele; (ii) men with idiopathic infertility; (iii) infertile men with chronic inflammatory urogenital tract diseases (IUTD); (iv) fertile men with IUTD and (v) men whose partners had a history of pregnancy loss. In the study population, the prevalence of viral DNA was 17.7, 3.4% for EBV, 5.2% for CMV, 6.5% for HHV-6, 0.43% for EBV + CMV, 0.87% for EBV + HHV-6 and 1.3% for CMV + HHV-6. The median viral loads for EBV, CMV and HHV-6 were 500, 2250 and 250 copies/mL respectively. Of the sperm cell fractions, derived from infected samples 87.5% contained viral DNA. No association between EBV and fertility disorders or IUTD was found. CMV detection was much higher in the group of patients with infertility and concomitant IUTD compared with the other groups combined (18.5% vs. 5.4%, p = 0.03) and associated with reduced sperm cell count (39.5 × 10(6) /mL vs. 72.5 × 10(6) /mL, p = 0.036). Immunostaining of spermatozoa from infected samples and in vitro-infected cells detected CMV in sperm heads, tails and connecting pieces and revealed attachment to sperm membrane and intracellular localization. HHV-6 was the more common in fertile men with chronic IUTD than in the other groups combined (19% vs. 6.3%, p = 0.018) and had no effect on sperm parameters. The results suggest that both CMV and HHV-6 may contribute to the aetiology of IUTD and, moreover, CMV-associated IUTD can lead to male sterility.

Herpesviruses are large, spherical, enveloped viral particles with linear double-stranded DNA genome. Herpesvirus virion consists of an icosahedral capsid containing viral DNA, surrounded by a protein layer called tegument, and enclosed by an envelope consisting of a lipid bilayer with various glycoproteins. Herpesviruses persist lifelong in their hosts after primary infection by establishing a latent infection interrupted recurrently by reactivations. The Herpesviridae family is divided into three subfamilies; α-herpesviruses, β-herpesviruses, and γ-herpesviruses based on the genome organization, sequence homology, and biological properties. There are eight human herpes viruses: Herpes simplex virus type 1 and 2 (HSV-1, −2) andVaricella-zoster virus (VZV), which belong to the α-herpesvirus subfamily; Human cytomegalovirus (HCMV), and Human herpesvirus type 6 and 7 (HHV-6,HHV-7), which belong to the β-herpesvirus subfamily; and Epstein–Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) or Human herpesvirus 8 (HHV-8), which belong to the γ-herpesvirus subfamily. Within this chapter, we summarize the current knowledge about EBV and CMV, regarding their genome organization, structural characteristics, mehanisms of latency, types of infections, mechanisms of immune escape and prevention. Epstein–Barr Virus (EBV) genome encodes over 100 proteins, of which only (30) proteins are well characterized, including the proteins expressed during latent infection and lytic cycle proteins. Based on major variation in the EBNA-2 gene sequence, two types of EBV are recognized, EBV type 1 and 2. Epstein–Barr virus types occur worldwide and differ in their geographic distribution depending on the type of virus. EBV spreads most commonly through bodily fluids, especially saliva. However, EBV can also spread through blood, blood transfusions, and organ transplantations. The EBV is associated with many malignant diseases such as lymphomas, carcinomas, and also more benign such as infectious mononucleosis, chronic active infection. The EBV has also been suggested as a trigger/cofactor for some autoimmune diseases. Overall, 1–1.5% of the cancer burden worldwide is estimated to be attributable to EBV The latently infected human cancer cells express the most powerful monogenic proteins, LMP-1 and LMP-2(Latent Membrane Protein-1,-2), as well as Epstein–Barr Nuclear Antigens (EBNA) and two small RNAs called Epstein–Barr Encoded Small RNAs (EBERs). The EBV can evade the immune system by its gene products that interfering with both innate and adaptive immunity, these include EBV-encoded proteins as well as small noncoding RNAs with immune-evasive properties. Currently no vaccine is available, although there are few candidates under evaluation. Human cytomegalovirus (HCMV) is a ubiquitous beta herpesvirus type 5 with seroprevalence ranges between 60 to 100% in developing countries. CMV is spread from one person to another, usually by direct and prolonged contact with bodily fluids, mainly saliva, but it can be transmitted by genital secretions, blood transfusion and organ transplantation. In addition, CMV can be transmitted vertically from mother to child. CMV infection can result in severe disease for babies, people who receive solid organ transplants or bone marrow/stem cell transplants and people with severe immune suppression such as advanced human immunodeficiency virus (HIV) infection. The HCMV has several mechanisms of immune system evasion. It interferes with the initiation of adaptive immune responses, as well as prevent CD8+ and CD4+ T cell recognition interfering with the normal cellular MHC Class I and MHC Class II processing and presentation pathways. Challenges in developing a vaccine include adeptness of CMV in evading the immune system. Though several vaccine candidates are under investigation.

Predictive Value of Quantitative PCR-Based Viral Burden Analysis for Eight Human Herpesviruses in Pediatric Solid Organ Transplant Patients