and inhibit host cell DNA replication and mRNA transcription. Poliovirus can inactivate proteins involved in host mRNA translation without affecting poliovirus mRNA translation. In some cases, expression of viral fusion proteins on the surface of the host cells can cause host cell fusion to form multinucleated cells. Notable examples include measles virus, HIV, respiratory syncytial virus. Importantly, viral infections can differ by the "lifestyle strategy". Persistent infections happen when cells continue to survive despite a viral infection and can be further classified into latent (only the viral genome is present, there is no replication occurring) and chronic (basal levels of viral replication without stimulating an immune response). In acute infections, lytic viruses are shed at high titres for rapid infection to a secondary tissue/host, whereas persistent viruses undergo shedding at lower titres for a longer duration of transmission (months to years). Lytic viruses are capable of destroying host cells by incurring and/or interfering with the specialised functions of host cells. An example would be the triggering of necrosis in host cells infected with the virus. Otherwise, signatures of viral infection, like the binding of HIV to co-receptors CCR5 or CXCR4, can also trigger cell death via apoptosis through host signalling cascades by immune cells. However, many viruses encode proteins that can modulate apoptosis depending on whether the infection is acute or persistent. Induction of apoptosis, such as through interaction with caspases, will promote viral shedding for lytic viruses to facilitate transmission, while viral inhibition of apoptosis could prolong the production of virus in cells, or allow the virus to remain hidden from the immune system in chronic, persistent infections. Nevertheless, induction of apoptosis in major immune cells or antigen-presenting cells may also act as a mechanism of immunosuppression in persistent infections like HIV. The primary cause of immunosuppression in HIV patients is due to the depletion of CD4+ T helper cells. Interestingly, adenovirus has an E1A protein to induce apoptosis by initiating the cell cycle, and an E1B protein to block the apoptotic pathway through inhibition of caspase interaction. Persistent viruses can sometimes transform host cells into cancer cells. Viruses such as the human papillomavirus (HPV), human T-lymphotropic virus (HTLV) etc., can stimulate growth of tumours in infected hosts, either by disrupting tumour suppressor gene expression (HPV) or upregulating proto-oncogene expression (HTLV). Damage caused by host immune system Sometimes, instead of cell death or cellular dysfunction caused by the virus,