Human EBV VCA IgM ELISA Kit

Epstein-Barr virus is a lymphotropic DNA virus of the genus Herpesvirus. It is found throughout the world, mostly sporadically, but can cause small epidemics. It can occur all year round, but is more common in late autumn and early spring. Fever, rash and swollen lymph nodes are typical symptoms. Epstein-Barr virus easily infects children aged 3-5 years. Most young children have no obvious symptoms after infection, or it may cause mild pharyngitis and upper respiratory tract infection. Primary infection occurs in adolescence and about 50% develop infectious mononucleosis. It is mainly spread by saliva but can also be transmitted by blood transfusion. The EB virus replicates in the epithelial cells of the oropharynx and then infects B lymphocytes. These cells enter the bloodstream in large numbers and cause systemic infection. It can also remain dormant in human lymphatic tissue for a long time. When the body's immune function is low, the latent EB virus is activated and can cause recurrent infection. EB virus (EBv), also known as human herpesvirus (HHV-4). EBv was first successfully identified by Epstein and Barr in 1964 by culturing Burkitt's African childhood lymphoma cells in vitro and observing herpes virus particles in the cell smears of the established strains under the electron microscope, hence the name Epstein-Barr virus. It can cause infectious mononucleosis and is closely associated with the development of Burkitt's lymphoma, nasopharyngeal carcinoma and various lymphomas. It was discovered by Epstein, Barr and others in tissue cultures of malignant lymphomas in African children and identified as the causative agent of this disease by Henle and others in 1968. It mainly invades B lymphocytes (B lymphocytes have C3 receptors on their surface, which are the same as EBV receptors). EB virus is round, with a diameter of 180nm. Its basic structure consists of three parts: nucleus, capsid and capsule. The nucleus is a dense substance with a diameter of 45nm, mainly containing double-stranded linear DNA. The viral capsid is a 20-sided symmetric type consisting of a total of 162 capsid particles. The capsid consists of the nuclear membrane of the infected cell. On the nuclear membrane there is a virally encoded membrane glycoprotein which has the function of recognizing EB virus receptors on lymphocytes and cell fusion. Viral nucleic acids are double-stranded DNA, usually inserted into the chromosomal DNA of host cells as linear molecules and present in free cells as circular molecules.

Figure 1. Epstein-Barr virus structure and infection of cells. (Sources: Houen G, et al. 2021)

EBV has five antigenic components, all of which can produce corresponding antibodies: 1. Capsid antigen (VCA): VCA IgM antibodies appear early and usually disappear after 1 to 2 months. They are an indication of recent EBV infection. VCA IgG appears slightly later, but can persist for many years or a lifetime, making it impossible to distinguish between recent and past infections. 2. Early antigen (EA): It can be further subdivided into the diffuse component D and the localized component R. It is an antigen produced when EBV enters the early stage of the proliferative cycle. The EA-D component has EBV-specific DNA polymerase activity. EAIgG antibody is a sign of recent infection or active EBV replication. The antibody peaks 3 to 4 weeks after disease onset and persists for 3 to 6 months. 3. Core antigen (EBNA): EBNA IgG appears 3 to 4 weeks after disease onset and persists for life. It is a sign of previous infection. 4. Lymphocyte-determined membrane antigen (LYDMA): This is a complement binding antibody. Its appearance and duration is the same as EBNAgG. It is also a sign of previous infection. 5. Membrane antigen (MA): This is a neutralizing antigen that can produce corresponding neutralizing antibodies. It has the same appearance and duration as EBNAgG

During primary EBV infection: EBVVCA IgM antibodies increase in the early stage, then decrease to undetectable levels, and almost simultaneously EBVVCA IgG levels increase, which can last for life; in the late stage of acute infection or recurrent infection, EBVEA IgG antibodies appear; in the late recovery period, EBV NA IgG antibodies are produced and can last for life. In patients with symptomatic infectious mononucleosis, the simultaneous detection of serological EBVVCA IgM, EBV VCA IgG and EBVNA IgG antibodies is of great importance in distinguishing patients in the recovery period from those in the acute infection period. Elevated EBVNA IgG antibody levels in patients with infectious mononucleosis indicate that the patient has entered the late recovery period from the early recovery period; elevated EBVVCA IgG antibody levels indicate acute infection, and elevated EBV VCA IgM antibody levels may indicate a transition from early infection to acute infection.

EBV VCA IgM Antibody
Epstein-Barr Virus Capsid Antigen IgM
Viral Capsid Antigen IgM (EBV)
EBV IgM VCA
EBV VCA IgM Antibodies
Epstein-Barr Capsid IgM
EBV Early IgM Antibody
EBV IgM (VCA)