Selected novel fusion proteins derived from hepatitis B virus (HBV) splice variants and their proposed role and/or effect on HBV replication

Splice variantNovel proteinSize (kDa)Proposed role/effect on HBV replicationReferences
Sp1HBSP10
  • Induces apoptosis

[75, 79, 80]
  • Prevents apoptosis

[81]
  • Associated with higher levels of HBV replication and severe liver fibrosis

[5]
  • Limits liver inflammation

[82]
  • Interacts with cellular factors

[8385]
  • Induces T-cell responses

[86]
p21.521.5
  • Inhibits nucleocapsid formation to reduce wild-type HBV replication

[88]
C-terminal truncated core protein21
  • Replaces wild-type core protein

[87]
  • Contributes to nucleocapsid formation

[1]
N-terminal truncated pol protein39
  • Unknown

[48]
Sp3Precore-pol48
  • Unknown

[9, 89]
Core-pol47
  • Unknown

[9, 89]
Sp7HBDSP15
  • Acts as a Gal4 activation domain

  • Has transactivation activity on viral genes

[76]
Sp9Precore-surface45
  • Strongly decreases wild-type HBV replication

[89]
Core-surface44
  • Strongly decreases wild-type HBV replication

[89]
C-terminal truncated pol with new open reading frame12
  • Unknown

[89]
N-terminal truncated pol50
  • Unknown

[89]
Sp10Core-surface35
  • Unknown

[78]
Sp13Pol-surface43
  • Replaces large surface protein

[90]
  • Prevents secretion of HBsAg

[77]
  • Involved in Sp13-mediated suppression of wild-type HBV replication

[77]

HBSP: hepatitis B spliced protein; pol: polymerase; HBDSP: hepatitis B doubly spliced protein; HBsAg: hepatitis B surface antigen