Properties of HHV (cont) Replication: Nuclear. Assembly: Nuclear. Common Antigens: None! Set up latent or persistent infection following primary infection Reactivation are more likely to take place during periods of immunosuppression Both primary infection and reactivation are likely to be more serious in immunocompromised patients
Properties of HHV (cont.) Replication: Nuclear. Assembly: Nuclear. Common Antigens: None! Set up latent or persistent infection following primary infection Reactivation are more likely to take place during periods of immunosuppression Both primary infection and reactivation are likely to be more serious in immunocompromised patients
Genomes of hhvs All HHV genomes have a unique long(UL)and a unique short(Us)region, bounded by inverted repeats The repeats allow rearrangements of the unique regions HHV genomes exist as a mixture of 4 isomers HHV genomes contain multiple repeated sequences. HSY("150kbp) YzY("120-130kbp) IRL IRS CMY (220kbp) U3 ‖ EBY("170kbp) IR4 DR TR
Genomes of HHVs All HHV genomes have a unique long (UL) and a unique short (US) region, bounded by inverted repeats. The repeats allow rearrangements of the unique regions HHV genomes exist as a mixture of 4 isomers. HHV genomes contain multiple repeated sequences
Human herpesviruses Name Common name associated diseases subfamily size HHV-1 Herpes Simplex Virus 1(HSV-1) 150kb Oral, ocular lesions; encephalitis HHV-2 Herpes simplex virus 2(HSV-2) c 150kb Genital oral lesions: neonatal infections HHV-3 Varicella Zoster virus(vzv) 130kb Chickenpox, shingles HHV-4 Epstein-Barr virus(EBV) 170kb Infectious Mononucleosis: BL NPC, NHL HHV-5 Human Cytomegalovirus(HCMV) 230kb Congenital infection systemic infection HHV-6 Human herpesvirus 6(HHV-6) 160kb Exanthem subitum; systemic infection HHV-7 Human herpesvirus 7(HHV-7) 160kb Exanthem subitum? HHV-8 Kaposis Sarcoma-herpesvirus(KSHV) 140kb Kaposis Sarcoma, B cell lymphomas
Human herpesviruses Name Common name associated diseases subfamily size HHV-1 Herpes Simplex Virus 1 (HSV-1) a 150kb Oral, ocular lesions; encephalitis HHV-2 Herpes Simplex Virus 2 (HSV-2) a 150kb Genital oral lesions; neonatal infections HHV-3 Varicella Zoster virus (VZV) a 130kb Chickenpox, shingles HHV-4 Epstein-Barr virus (EBV) g 170kb Infectious Mononucleosis; BL, NPC, NHL HHV-5 Human Cytomegalovirus (HCMV) b 230kb Congenital infection; systemic infection HHV-6 Human herpesvirus 6 (HHV-6) b 160kb Exanthem subitum; systemic infection HHV-7 Human herpesvirus 7 (HHV-7) b 160kb Exanthem subitum? HHV-8 Kaposi’s Sarcoma-herpesvirus (KSHV) g 140kb Kaposi’s Sarcoma, B cell lymphomas
The herpesvirus family highly co-evolved with host widely disseminated from human to flog fish and snake Alpha herpesviruses Fast replication, cytolytic; latent in neurons (Herpes Simplex, Varicellar Zoster) Beta herpesviruses Intermediate replication, cytomegalic; latent in glands, kidneys(Cytomegalovirus, HHV-6,-7) · Gamma herpesviruses Slow replication, latent in lymphocytes lymphoproliferative, (Epstein-Barr virus, HHV-8)
The Herpesvirus Family highly co-evolved with host widely disseminated from human to flog, fish and snake • Alpha herpesviruses – Fast replication, cytolytic; latent in neurons (Herpes Simplex, Varicellar Zoster) • Beta herpesviruses – Intermediate replication, cytomegalic; latent in glands, kidneys (Cytomegalovirus, HHV-6, -7) • Gamma herpesviruses – Slow replication, latent in lymphocytes, lymphoproliferative, (Epstein-Barr virus, HHV-8)
What is Latency AND Why there is latency? At cellular level, Latency is the reversibly nonproductive infection of a cell by a replication-competent virus (1) They can successfully evade the host immune response (2) They enable their genome to persist in the latently infected cell, thereby in the host (3)They co-exist with the host cells and the host. (4 The host becomes a active carrier for transmission. All HHVs are capable of establishing latent infection Please note: The difference with abortive infection or infection with defective virus
At cellular level, Latency is the reversibly nonproductive infection of a cell by a replication-competent virus. (1) They can successfully evade the host immune response. (2) They enable their genome to persist in the latently infected cell, thereby in the host. (3) They co-exist with the host cells and the host. (4) The host becomes a active carrier for transmission. All HHVs are capable of establishing latent infection. Please note: The difference with abortive infection or infection with defective virus. What is Latency? AND Why there is latency?