Category Archives: Structure of Virus

Japanese Encephalitis (JE) Virus: Structure, life cycle, pathogenesis and diagnosis

Japanese Encephalitis (JE) Virus was initially isolated in Japan in 1935. It is a leading cause of vaccine-preventable encephalitis in Asia and the western Pacific.

Fig: Geographic Distribution of Japanese Encephalitis Virus

Fig: Geographic Distribution of Japanese Encephalitis Virus

The virus is maintained in an enzootic cycle between mosquitoes and amplifying vertebrate hosts. The highest risk months for JE transmission are August, September and early October


  • Falls under Arboviruses (Alpha viruses, Flaviviruses, Bunya viruses)
  • member of the family flaviviruses
  • related to dengue, yellow fever and West Nile viruses, Saint Louis encephalitis viruses.
  • +ve stranded SS RNA Virus
  • linear non-segmented genomes
  • icosahedral shaped
  • Envelope is present

Measles virus: structure, pathogenesis, clinical feature, complications and lab diagnosis

The name measles is derived from the Latin, misellus, meaning miserable.

  • Measles (also called Rubeola-(from rubeolus, Latin for reddish) ) is usually a disease of childhood (aged 3-10 years) and is followed by life-long immunity.
  • Important cause of childhood  mortality in developing countries.
  • Human is the natural host

Structure of Measles Virus

  • Measles virus is a member of the genus Morbillivirus of the family Paramyxoviridae. Paramyxoviruses are so called because they have an affinity for mucous membranes (Greek: myxa = mucus).

    Structure of Measles Virus

    Structure of Measles Virus

  • Measles virus is a typical paramyxovirus (spherical enveloped particles that contain a non segmented negative strand RNA genome with a linear arrangement of genes)
  • Measles virus have two glycoproteins  spikes that are important in pathogenesis:
    • F (fusion) protein, which is responsible for fusion of virus and host cell membranes, viral penetration, and haemolysis, and the
    • H (haemagglutinin) protein, which is responsible for binding of virus to cells

How does the influenza virus change so fast?

Influenza has two ways to change — one slow and one fast. The slow change is called “drift” — the virus gradually accumulates individual mutations until its surface proteins are no longer recognized by our immune system.

The fast change is called “shift” — different strains of influenza can exchange genetic material if they infect the same cell at the same time. A new “hybrid” strain can emerge with surface proteins that are completely different from the previous year’s epidemic strain.

To picture shift and drift, it helps to know a little bit about influenza virus genetics.

Why does influenza come back year after year?

After an epidemic, shouldn’t everyone be immune to the virus? Why is influenza able to come back again and again? The answer lies in the virus’s genetic structure and high mutation rate. The truth of the matter is that an individual’s immune system rarely sees the same influenza virus twice and that means it cannot provide the permanent protection it offers against more stable infectious agents.

Whenever you are infected by a pathogen, your immune system generates compounds called antibodies that bind to the infectious agent and target it for destruction. After the infection is cured, a few of the white blood cells that make those specific antibodies continue to circulate in your blood. Called “memory cells”, these cells are quickly activated 

Structure clinical feature and Lab diagnosis of Herpes Simplex Virus

Herpes Simplex viruses are members of the Alphaherpesvirinae subfamily of human herpesviruses together with varizella-zoster virus (VZV), also called human herpesvirus. HSV is a large virus with a core containing double-stranded DNA within a coat, an icosahedron with 162 capsomeres. The envelope which surrounds the ‘naked’ particle is partly nuclear membrane derived, partly virally coded, with glycoprotein spikes. The diameter of a complete particle is 120–200 nm. The ‘naked’ virion measures about 100 nm.
The virus enters the cells through cellular membrane fusion after being attached to specific receptors through an envelope glycoprotein. The capsid is transported to nuclear pores where DNA circularizes after uncoating, and enters the nucleus. The genome is a 120–230 kbp double-stranded, linear DNA with repeated sequences located at each flank and certain other regions. Genomic rearrangements giving genomic ‘isomers’ may occur, but the biological significance of this is unknown. HSV1 and HSV2 show 50% sequence homology.