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Congenital cytomegalovirus is a group of symptoms that occur when an infant is infected with the cytomegalovirus (CMV) before birth. Causes Congenital cytomegalovirus occurs when an infected mother passes CMV to the fetus through the placenta.
Infection caused due to Viruses can be very dangerous for babies and other people with weak Immune System.
Cytomegalovirus can be spread through contact with the above mentioned fluids and if you touch these fluids first with hands then touch your face or body etc. Most of the time, Cytomegalovirus is resolved on its own but sometimes, this disease can be life threatening. If you weak Immune system and you are suffering from the above mentioned symptoms of CMV, you should urgently consult a doctor.
If you are Pregnant and you are suffering from Mononucleosis, then you should consult a doctor for the diagnosis of CMV infection. If you are healthy but you are suffering from symptoms of Cytomegalovirus, you can be in the re-activation period. Newborn babies and other people with weak Immune System, require a treatment when they suffer from the symptoms of CMV infection like Pneumonia.
Try to wash the Hands with Soap and Water after changing diapers of children, vomit or Saliva etc. Try to kiss the Forehead of a Child, instead of kissing Lips of an infected child especially, when you are Pregnant. Be careful when you are disposing Diapers, tissues and other things that have body’s fluid on them. If you have Compromised Immune System, Anti-Viral medicines can help in preventing this disease to a large extent. Ganciclovir, a synthetic acyclic nucleotide analog of guanine, is phosphorylated to a triphosphate within the cell and acts as an inhibitor of viral DNA synthesis. Children with congenital CMV infection are at risk for hearing loss, mental retardation, psychomotor delay, cerebral palsy, and impaired vision. Women of childbearing age should practice meticulous personal hygiene, such as avoidance of contact with urine or saliva of others and proper hand-washing after such contact. This program is funded through Health Resources and Services Administration, US Department of Health and Human Services. Describe the clinical manifestations and retinal findings in patients with cytomegalovirus retinitis. Discuss appropriate treatment options for patients with newly diagnosed cytomegalovirus retinitis.
Which one of the following statements is TRUE related to CMV retinitis in HIV-infected patients? Cytomegalovirus (CMV) retinitis in HIV-infected patients usually results from reactivation disease in persons previously infected with CMV.CorrectCytomegalovirus (CMV) retinitis in HIV-infected patients almost always represents reactivation of CMV (with dissemination) in persons with latent CMV infection. The diagnosis of CMV retinitis should be confirmed in all patients with suspected CMV retinitis by detecting CMV (using PCR-based techniques) in vitreous fluid.IncorrectThe diagnosis of CMV retinitis is based on characteristic funduscopic findings observed during a dilated funduscopic examination by an ophthalmologist. Figure 1Figure 1 - Retinal Anatomic ZonesThis illustration shows a schematic representation of an entire retina with superimposed anatomic zones (as defined by the UCLA CMV Retinopathy Study Group).
Figure 2Figure 2 - Normal RetinaThis image of a normal retina identifies important landmarks visible with a hand-held ophthalmoscope.
Figure 3Figure 3 - Cytomegalovirus Retinitis, Central Portion of RetinaThis retinal photograph taken from an AIDS patient with cytomegalovirus retinitis shows an opacified, edematous retina (yellow) and hemorrhage (red); the retinitis involves the optic nerve head and extends adjacent to the macula along the retinal blood vessels.
Figure 4Figure 4 - Cytomegalovirus Retinitis, Brushfire PatternThis retinal photograph taken from an AIDS patient with cytomegalovirus retinitis shows extensive retinitis in a brushfire pattern in the upper and right region of the image.
Figure 5Figure 5 - Cytomegalovirus Retinitis, Smoldering LesionThis retinal photograph is taken from an AIDS patient in whom cytomegalovirus retinitis (arrow) developed in a slower fashion ("smoldering CMV retinitis"). Figure 6Figure 6 - HIV RetinopathyThis retinal photograph taken from a patient with HIV retinopathy shows multiple "cotton wool spots". Figure 8Figure 8 - Ganciclovir Implant Before and After Intraocular Insertion The right part of the figure shows a ganciclovir sustained release implant; this implant contains ganciclovir embedded in a polymer-based system that slowly releases the drug.
Multiple therapies have been studied and established as effective for initial therapy of acute CMV retinitis, including intravenous ganciclovir (Cytovene),[8,9] intravenous foscarnet (Foscavir),[10] intravenous cidofovir (Vistide),[11,12] oral valganciclovir (Valcyte),[9]  sustained release ganciclovir intraocular implant (Vitrasert) alone or with oral ganciclovir (Cytovene),[8,13,14] and intravitreal ganciclovir or foscarnet.[15,16] Although oral ganciclovir was used in some of the earlier studies (and shown to have some efficacy), oral valganciclovir has completely replaced oral ganciclovir in clinical practice. Patients undergoing treatment for CMV retinitis require close follow-up by an ophthalmologist experienced in managing CMV retinitis and by an HIV provider. After the 14 to 21 days of initial therapy, patients should transition to maintenance therapy (Figure 10). This editable Main Article is under development and not meant to be cited; by editing it you can help to improve it towards a future approved, citable version. Cytomegalovirus, CMV, is a member of the family of human herpesviridae1 , and is known as human herpesvirus 5 (HHV-5).
CMV is a virus which can produce congenital[4] and acquired infection, and has therefore become an important pathogen of study. Human Cytomegalovirus strains were isolated by three independent scientists: Smith and Rowe in 1956 and Weller in 1957. CMV is structurally similar to other herpesviruses in that it has an icosahedral [9] capsid [10]surrounding and protecting the genetic material.
CMV is a virus which affects many species including humans, monkeys, and rodents, and can be found in almost all organs of the host. Although the host has the ability to defend itself against a CMV invasion, CMV has the ability to evade the host immunity, and in this way, it can cause infection in the host.
The second type of CMV disease occurs after this initial infection, and is a reactivation of the latent CMV.
When the host is infected, CMV DNA can be detected with polymerase chain reaction (PCR)[27] in all the different cell lineages and organ systems in the body. Currently, there is no vaccine for CMV, but preventative measures can be taken to keep from getting the virus.
Researchers first tested its virulence because they wanted to make sure that these mutant CMV's would not be dangerous.
Does Cytomegalovirus Develop Resistance following Antiviral Prophylaxis and Treatment in Renal Transplant Patients in Kuwait? The mother's illness may not have symptoms, so she may be unaware that she has CMV. Symptoms Most congenitally infected children do not have symptoms. Most of the people, who suffer from CMV don’t even know, they suffer from this disease because sometimes, they don’t get sick. Other tests can find Virus in Blood. Body Fluid is also used or Tissue Biopsy is done to detect the disease. These Vaccines can be beneficial in the prevention of CMV infection in both mothers and the babies.
If you have anyone around you suffering from this disease, do take care of them but with proper care so that it might not affect you as well. Preliminary data have shown ganciclovir effective in the treatment of symptomatic congenital CMV infection. This is especially so for the hearing loss, for as many as 80% of cases are of late-onset or progressive. Nurses who practice good handwashing do not have increased rates of CMV acquistition, but daycare workers often do, suggesting that barrier precautions are effective in interrupting transmission. She describes difficulty seeing out of her left eye and she has noticed many floaters in the same eye.
Most experts would recommend treatment with intravitreal injections with ganciclovir or foscarnet, in combination with oral valganciclovir (Valcyte) or intraveneous ganciclovir (Cytovene).The optimal time to initiate antiretroviral therapy in patients with acute CMV retinitis has not been clearly established. Visual loss is a common initial presenting symptom and is often first detected as a visual field deficit. Using a standard direct ophthalmologic examination, only a small portion of the retina is visualized (all of zone 1 and some of zone 2). The macula is in the center of the retina; it contains densely packed cones that specialize in visual acuity and color vision.
In the area farthest to the upper right, retinal necrosis and atrophy have lead to retinal pigment epithelial change, as evident by the darkly pigmented appearance. This "smoldering" type of lesion often does not cause noticeable symptoms, and may escape detection until it extends closer to the site-threatening region (zone 1). These "cotton wool spots" represent nerve fiber layer infarcts, identical to those often seen in patients with hypertension or diabetes mellitus. The left part of the figure shows the implant following insertion into the vitreous chamber of the eye.
Preferred and Alternative Regimens for Acute CMV RetinitisSource: Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. Preferred and Alternative Regimens for CMV Chronic Maintenance TherapySource: Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents.
As the retinitis expands, it takes on a brushfire pattern, with an active white or yellow leading edge and a darker, atrophic, scarred area present behind the active edge (Figure 4).


In addition, studies have shown that oral valganciclovir alone is at least as effective as intravenous ganciclovir (Figure 7).[9] The ganciclovir implant (Figure 8) provides sustained local (intraocular) release of ganciclovir for 6 to 8 months, and demonstrated excellent efficacy in several studies,[8,13,14] but unfortunately it is no longer commercially available in the United States.
Guidelines for the treatment of cytomegalovirus diseases in patients with AIDS in the era of potent antiretroviral therapy: recommendations of an international panel.
Incidence and natural history of cytomegalovirus disease in patients with advanced human immunodeficiency virus disease treated with zidovudine.
Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. Correlation between CD4+ counts and prevalence of cytomegalovirus retinitis and human immunodeficiency virus-related noninfectious retinal vasculopathy in patients with acquired immunodeficiency syndrome. Changes in the natural history of cytomegalovirus retinitis following the introduction of highly active antiretroviral therapy. Risk of vision loss in patients with cytomegalovirus retinitis and the acquired immunodeficiency syndrome. Learning about it, its phylogenetic history, and its genome gives us a greater understanding of the organism and can lead to the development of a working drug against this ubiquitous virus. It is more the 240 kilobase pairs [7]long making it the largest member of the herpesvirus family. This genome contains two unique sequences, a long unique sequence and a short unique sequence.
It has become a very efficient virus because it has evolved mechanisms to remain undetected in its environment.
CMV has genes that interfere with the antigen presentation of infected cells, thus limiting the immune response to it. If a person becomes immunocompromised, for example someone with HIV, someone who received an organ or bone marrow transplant [20], or even someone under a lot of stress, the virus can flare up again. This is when a woman who is infected with CMV (even if she doesn't have any symptoms) passes it to her child. If a newborn or immunocompromised patient is infected, or someone has more serious symptoms, antiviral intravenous drugs may be used.
The best way to prevent from becoming infected with CMV is frequent hand washing, avoiding sharing drinking glasses, and avoiding contact with bodily fluid, especially of young children.
Presently, there is no vaccine for CMV and this can become a problem especially for pregnant and nursing women, and for immunocompromised people. De Clerq, “New inhibitors of human cytomegalovirus (HCMV) on the horizon,” Journal of Antimicrobial Chemotherapy, vol. It is linked to the Viruses that can originate Chickenpox and other Mononucleosis infections. Most of the people don’t know that they are suffering from CMV because it hardly shows some symptoms. The Cytomegalovirus is linked to the Virus that causes Chickenpox, Herpes, Simplex and Mononucleosis.
A phase II study with ganciclovir showed hearing improvement or stabilization in five of 30 infants with symptomatic congenital CMV infection at six months or later. As such, children with congenital CMV infection should have long-term audiologic, neurodevelopmental, and ophthalmic follow-up for early identification of these problems. Approximately 1-year prior, she was diagnosed with HIV infection and has refused to regularly engage in medical care for management of her HIV disease. The implant is inserted in the operating room and requires a simultaneous partial vitrectomy. Patients do not have pain related to the lesions, nor do they present with redness of the eye.
In some instances, patients can have smoldering lesions outside of zone 1 that may be more difficult to diagnose (Figure 5).
Primarily because of its toxicity, intravenous foscarnet is generally reserved for patients who cannot tolerate oral valganciclovir or for those who have resistant or refractory disease. All systemic agents used to treat CMV retinitis have major toxicities and require laboratory monitoring.
Its classification as a herpesvirus is based on its tendency to infect mononuclear cells and lymphocytes 2 and on its molecular phylogenetic[3] relationship to other herpesviruses.Its classification as a betaherpesvirus is based on its long replication cycle, cytopathology, and restricted host range, which are all characteristic of the betaherpesviruses.
It can also be found in body fluids, including semen, saliva, urine, feces, breast milk, blood, and secretions of the cervix. It is capable of encoding more than 200 potential protein products, but the function of most of these proteins is presently unknown.
This capsid is made out of 162 hexagonal protein capsomeres [11], and is surrounded by a lipid bilayer [12]outer enevelope.
For example, the human cytomegalovirus has three genes which allow it to evade human immunity [14]. If this occurs, the symptoms can be more serious and include pneumonia [21] , hepatitis [22], encephalitis [23], myelitis [24], colitis [25], retinitis (inflamation of the retina), and neuropathy [26] . DEAFF or Detection of early antigen fluorescent foci is a method used for the early diagnosis of CMV infection. In this experiment, researchers wanted to construct a cell, which would not be pathogenic, but which would cause an CMV immune response. Even if a person doesn't have symptoms, he can pass the virus on through the saliva because CMV replicates for a long time in the salivary gland. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractThe resistance of cytomegalovirus (CMV) to ganciclovir or valganciclovir is a factor in therapeutic failure and disease progression. About 50 to 80% people in the United States, suffer from this disease mostly in the age of 40 years. She takes trimethoprim-sulfamethoxazole (Bactrim, Septra) for Pneumocystis pneumonia prophylaxis, but she takes no other medications and has never taken antiretroviral medications. The retina lines most of the inner wall of the back of eyeball and it is comprised of thin, multi-layered neural tissue; the retina receives and transmits images. The optic nerve functions to transmit impulses from the retina to the brain and the visible portion of the optic nerve is known as the optic nerve head or optic disc.
In addition, other lesions can be misdiagnosed as CMV retinitis, including HIV-associated retinopathy (Figure 6), toxoplasmosis, and varicella-zoster retinitis. During initial induction therapy, patients receiving ganciclovir, valganciclovir, or foscarnet should have twice weekly monitoring of complete blood counts, serum electrolytes, and renal function. It has the US3 gene whose products prevent the major histocompatibility complex [15] molecules from moving to the membrane. The CMV has certain genes that give the virus the ability to evade the host's immune system. They also want to test to see if the mutant CMV has the ability, like wild type CMV to remain dormant and then reactivate. They did this by constructing a plasmid with CMV genes that cause immune response in the host. Long after it replicates in the liver and spleen, it can be detected in the salivary glands for as long as months after the initial infection.
CMV strains resistant to ganciclovir or valganciclovir have been associated with specific mutations in the UL97 and UL54 genes. Once you get affected from this disease, it stays with you for rest of the life but sometimes it remains inactive. July 8, 2013.Figure 10Figure 10 - Maintenance Therapy for Cytomegalovirus RetinitisImage B. Zone 2 extends from the edge of zone 1 to a circle defined by the ampullae of the vortex veins.
In general, laboratory tests, such as CMV serology, antigen detection, PCR, or viral blood cultures, do not play a role in the acute evaluation in this setting.
Different strains have slightly different genomes, but all strains share about 80% of the genome. The US6 gene products inhibits peptide translocation of proteins involved with antigen [16] presentation. If symptoms are present, they are similar to those of mononucleosis, and include fever, fatigue, and muscle pain.
They do this by interrupting the processing and presentation of antigens on the surface of infected cells.
So researchers injected mice with mutant CMV and then killed their immune system with gamma radiation.
So, since glycoprotein B and phosphoprotein 65 are molecules in CMV that cause an immune response in the host, researchers constructed two plasmids, one with the gene for gB and the other with the gene for pp65. It is not known exactly how the CMV remains latent in the salivary gland, but it has been associated with its ability to interfere with and inhibit the activation of CD4 and CD8 cells. That way, any growth and development problems can be identified early, and treated promptly. Prevention Cytomegalovirus is almost everywhere in the environment.


A phase III randomized trial suggests that ganciclovir may benefit infants with severe congenital CMV infection. She is urgently referred to an ophthalmologist for evaluation of suspected cytomegalovirus (CMV) retinitis. Rating Scheme for 2013 Opportunistic Infections GuidelinesSource: Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. Zone 3 extends from the edge of zone 2 to the ora serrata and includes the area of attachment of the vitreous base.[1,6] Zone 1 (central) lesions are considered as immediate sight-threatening, and typically these lesions have affected central vision or may rapidly do so. In routine cases, it is not necessary to obtain a retinal biopsy or attempt to identify CMV in the eye to make the diagnosis. The US11 gene products move the class I heavy chain of the antigen from the endoplasmic reticulum to the cytosol, making it nonfunctional.
Histopathology- Cells infected with CMV are enlarged and have inclusion bodies which can be recognized from biopsy material.
Without antigens on infected cells, the body doesn't know that the cell is infected, and does not build up immunity to the virus. They injected these plasmids into cells via electroporation, making virus like replicon particles.
Sequencing results showed no specific mutations in either UL97 or UL54 gene of CMV and therefore the CMV strains in kidney transplant patients who received ganciclovir either prophylactically or therapeutically were from the wild type. Central nervous system damage that has already occurred will not be reversed, but ongoing viral replication causing postnatal damage is controlled campared to untreated CMV-infected controls.
Patients with retinitis beginning outside of the central (zone 1) region often have absence of any major symptoms, except for a peripheral field defect.
The virus therefore has the ability to survive in a host, without causing an immune response. To test the immune response to the mutant CMV, researchers measured CD8 responses, and to measure protective immunity, they immunized mice with mutant CMV and then introduced wild type CMV.
This article suggests a different way which CMV has the ability to replicate so well in the salivary glands.
Our results suggest that CMV management and immunosuppression protocols for kidney transplant patients followed in the Organ Transplant Centre, Kuwait, is very effective in reducing the opportunity of developing CMV antiviral resistance.1. The value of ganciclovir for the prevention or treatment of hearing loss in asymptomatic children has not been determined. If an infected cell can't present an antigen, then the body does not know that it is infected, and will not provide immunity against the virus. In this experiment, researchers deleted the genes that allow CMV to evade host immunity, from mouse CMV. They saw that the immunity that they had build towards mutant CMV was useful in fighting off wild type CMV infection. Researchers observed that persistent MCMV replication in the salivary glands was accompanied by the appearance of immunosupressive cytokine IL-10–expressing CD4 T cells, specifically within this organ, but not anywhere else.
IntroductionAt present, ganciclovir (GCV) and valganciclovir (VGCV) are the treatment of choice of cytomegalovirus (CMV) in case of infection in solid organ transplant (SOT) recipients [1, 2], and their use has led to a decline in the CMV disease and associated morbidity in SOT recipients [3].
Side effects of ganciclovir include bone narrow suppression and potential gonadal toxicity. Without the genes, the CMV would not have the ability to interrupt antigen presentation, and with antigens present, the immune system will recognize infected cells and be able to fight them. After the injections researchers found that mice immunized with gB VRP developed anti gB antibodies, which indicates a humoral immune response. Blockading signaling with this mechanism decreased the viral replication at this site, indicating that viral replication is due to the presence of the IL-10. However, with the advent of widespread and prolonged use of antiviral drugs for CMV prophylaxis and the use of immunosuppressive drugs, antiviral-resistant CMV mutants are emerging and are associated with disease progression [4].
Presently there is insufficient data to justify the routine use of ganciclovir in the treatment of congenital CMV infection. By doing this, the body would be building up immunity to a non pathogenic version of the virus, so in case he gets infected with the actual wild type virus, he will already have immunity to the virus.
They also saw that mice immunized with pp65 VRP developed robust T cells indicating a cellular immune response to the VRP. Researchers increased the ratio of CD4 T cells expressing IFN-? compared with those expressing IL-10 in the salivary glands. This reduced viral replication, further evidence that CMV replication in the salivary gland is due to the presence of IL-10. By increasing the amount of CD4 cells expressing IFN-?, and decreasing those that express IL-10, the CMV won't have the proper environment for its persistent replication, thus inhibiting its ability to remain latent for long periods of time. Wellington, “Valganciclovir: a review of its use in the management of CMV infection and disease in immunocompromised patients,” Drugs, vol.
Hamilton, “Cytomegalovirus infection following liver transplantation: review of the literature,” Clinical Infectious Diseases, vol. After cycle sequencing reactions, sequence analysis of UL97 and UL54 genes of CMV was performed using the automated DNA sequencer CEQ 8000 Genetic Analysis System DNA sequencer (Beckman Coulter, USA) as described by the manufacturer’s manual. Boeckh, “Emergence of ganciclovir-resistant cytomegalovirus disease among recipients of solid-organ transplants,” Lancet, vol.
Response of Patients to Antiviral TreatmentThe 54 CMV PCR positive kidney transplant patients were treated with either GCV or VGCV alone or a combination of the two drugs for a period ranging between 2-3 weeks and 3 months. During the treatment period, the patients were monitored regularly by measuring viral load in their plasma using the QPCR. Forty-eight patients responded well to therapy as indicated by the complete clearance of the virus from the bloodstream at the end of the therapy. Table 3 shows in detail the effect of the antiviral treatment on the viral load in the plasma samples of these 6 patients.
Among the 6 patients, 2 patients were treated according to prophylaxis protocol and 4 were treated according to therapeutic protocol. Li et al., “How evolution of mutations conferring drug resistance affects viral dynamics and clinical outcomes of cytomegalovirus-infected hematopoietic cell transplant recipients,” Journal of Clinical Microbiology, vol.
Patients 5 and 6, however, had severe form of CMV disease such as diarrhoea, bleeding, and renal failure and failed to respond well to therapy as there were no significant reductions in the viral load after treatment. Clinical PresentationThe above 6 patients had CMV-related symptoms and were CMV DNA positive by PCR for more than one-month long period and they did not show significant decreases in viral load despite antiviral treatment. CMV DNA was isolated from samples of these patients and were processed for sequence analysis to determine whether GCV or VGCV treatment had resulted in mutations in the CMV UL97 or UL54 genes.
Nampoory, “Detection and monitoring of cytomegalovirus infection in renal transplant patients by quantitative real-time PCR,” Medical Principles and Practice, vol. Jordan et al., “Analysis of the UL97 phosphotransferase coding sequence in clinical cytomegalovirus isolates and identification of mutations conferring ganciclovir resistance,” Journal of Infectious Diseases, vol.
Erice, “Resistance of human cytomegalovirus to antiviral drugs,” Clinical Microbiology Reviews, vol. Rollag et al., “Cytomegalovirus resistance in solid organ transplant recipients treated with intravenous ganciclovir or oral valganciclovir,” Antiviral Therapy, vol. Drew, “Viral DNA polymerase mutations associated with drug resistance in human cytomegalovirus,” Journal of Infectious Diseases, vol. Chou, “Sequencing of cytomegalovirus UL97 gene for genotypic antiviral resistance testing,” Antimicrobial Agents and Chemotherapy, vol.
Boivin, “Resistance of herpesviruses to antiviral drugs: clinical impacts and molecular mechanisms,” Drug Resistance Updates, vol. Emery, “Investigation of CMV disease in immunocompromised patients,” Journal of Clinical Pathology, vol.
Boivin et al., have also detected multiple UL54 mutations of unknown significance in clinical strains isolated from SOT recipients [10]. One possible explanation of the absence of drug resistance mutants in our patients is that generally, the incidence of CMV drug resistance in kidney transplant recipients is known to be rather low when compared with the incidence of drug resistance in other solid organ transplant (SOT) and AIDS patients [11]. In a study by Lurain et al., on CMV isolates from SOT patients, it is likely that the incidence of resistance in lung-transplant recipient is higher than other recipient and the incidence of resistance in kidney transplant is rather low [12, 13]. Griffiths, “Human cytomegalovirus (HCMV) replication dynamics in HCMV-naive and -experienced immunocompromised hosts,” Journal of Infectious Diseases, vol.
In summary, after the start of therapy, different rates of clearance of CMV are likely to occur due to a combination of different factors including host and virus factors and may not be related only to the presence of drug resistance mutants.
Caliendo, “Cytomegalovirus (CMV) virus load kinetics to predict recurrent disease in solid-organ transplant patients with CMV disease,” Journal of Infectious Diseases, vol. Limaye, “Ganciclovir-resistant cytomegalovirus in organ transplant recipients,” Clinical Infectious Diseases, vol.



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  • ILQAR007, 09.09.2015 at 14:17:30
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