EBV infections are caused by the EBV virus and occur mostly in childhood. Most have a good prognosis, except for immunodeficient individuals whose infection can be life-threatening. EBV has been found to be associated with certain tumors such as nasopharyngeal carcinoma, Burkitt’s lymphoma, and certain autoimmune diseases such as rheumatoid arthritis and dry syndrome. Clinical manifestations 1. Asymptomatic or atypical infections are most often seen in young children. The manifestations are often mild, such as upper respiratory tract infection, tonsillitis, persistent fever with or without lymph node enlargement. 2. Acute infectious mononucleosis is a typical manifestation of primary EBV infection. It is mostly seen in older children and adolescents. There are often 3-5 days of prodromal manifestations: headache, malaise, malaise, fear of food, etc., followed by the following typical signs: (1) Fever, pharyngitis, lymph node enlargement triad: almost all have fever, body temperature is often ≥ 39.5 ℃, lasting about 10 days, and then gradually drop to normal. Pharyngitis is seen in about 80% of children and occurs within the first week of illness, often exudative. 90% of children have rapid enlargement of superficial lymph nodes shortly after onset of illness, which can involve the whole body, with the most obvious involvement of the neck. (2) Splenomegaly: Splenomegaly occurs within 3 weeks of disease in about 50% to 70% of cases and is soft in texture. Rupture of the spleen is rare, but is a serious complication, so heavy pressure should not be applied when examining the spleen. (3) Hepatomegaly and abnormal liver function: In IM, temporary increase of liver enzymes occurs in about 40% or more cases, mostly in the range of 45-300 U/L, with a few reaching 500 U/L or more. Hepatomegaly is seen in 30% to 50% of children, and is more common in children under 4 years of age. About 2% to 15% are accompanied by jaundice. Liver function can be completely restored within 2 weeks to 2 months. It usually does not cause chronic liver disease. (4) Other manifestations: rash may appear in young children and abdominal pain may be seen in older children or adolescents. In addition, hematologic (anemia, thrombocytopenia, granulocytopenia), pulmonary (pneumonia), neurologic (encephalitis, meningoencephalitis, Guillain-Barre syndrome, peripheral facial palsy), cardiovascular (myocarditis, pericarditis) and renal (glomerulonephritis) complications are rare. (5) Typical blood picture: It appears within 1-4 weeks after the disease. The main manifestations are lymphocytosis ≥ 50% and heterogeneous lymphocytosis ≥ 10%, and a white blood cell count of 10-20×109/L. If there are no complications, the course of the disease is usually 2-4 weeks, and may occasionally extend to several months. 3. EBV infection in children with immunodeficiency mainly refers to children with X-linked lymphoproliferative syndrome (XLP) and acquired immunodeficiency. Lethal mononucleosis,? secondary hypo- or no immunoglobulinemia, malignant polyclonal-derived lymphoma, aplastic anemia, and chronic lymphocytic interstitial pneumonia. The morbidity and mortality rate is as high as 60%. Pathogenic diagnosis 1. Serological examination: Positive anti-VCA IgG indicates that one has been infected or is infected with EBV. Since its peak is in the acute phase, there is little value in observing double copies of serum to diagnose acute primary infection. Anti-VCA IgM appears early in the disease and disappears in about 2-3 months and is an indicator of acute primary infection. anti-VCA IgM levels in children under 4 years of age are low and disappear quickly (often within 3-4 weeks after the disease). In chronic or recurrent infections, anti-VCA IgG is high titer; anti-EA is often increased; anti-EBNA is positive (occasionally undetectable); and anti-VCA IgM is usually negative. 2. Viral marker detection: EBV DNA detection by nucleic acid hybridization and PCR in saliva or oropharyngeal washings in exfoliated epithelium, lymphatic tissue and tumor tissue is the most specific detection method. Immunolabeling techniques can also be used to detect viral antigens in the sample, such as EBNA, latent membrane antigen (one of the components of LYDMA). 3. Virus isolation: Virus isolation and identification is performed using the property that EBV infection causes unlimited proliferation of cultured B cells (human umbilical cord blood or peripheral lymphocytes). It takes 6 to 8 weeks. 4.Anti-anisotropic antibodies: The presence of anisotropic antibodies, i.e. IgM antibodies, in the patient’s serum can assist in the diagnosis, and are rarely positive in children under 4 years of age. Treatment 1.Supportive symptomatic treatment: bed rest is needed in the acute stage, corresponding treatment such as antipyretic, analgesic, liver protection, etc. Short-term corticosteroids can be used cautiously in patients with severe symptoms of transmission. If secondary streptococcal infection is confirmed by pharyngeal swab culture or antigen testing, additional sensitive antibiotics are required. Those with splenomegaly should avoid significant physical activity or exercise during the recovery period to prevent splenic rupture; emergency surgical management or non-surgical treatment should be given in case of splenic rupture. Tracheal intubation is recommended in cases of complete airway obstruction due to deep upper respiratory tract inflammation. 2, antiviral therapy: there is a lack of antiviral drugs with significant efficacy against EBV infection, and nucleoside analogues such as ganciclovir have an inhibitory effect on EBV, but there is a lack of suitable clinical studies to evaluate. Preliminary studies have shown some efficacy in severe EBV-induced lymphoproliferative disease using anti-B-cell monoclonal antibodies and irradiated transplanted donor leukocytes, while reducing the dosage of immunosuppressive agents.