Can all types of vaccines be given on the same date?

Administration of different vaccines at the same visit both live and inactivated vaccines does not result in decreased antibody responses or increased rates of adverse reaction. Simultaneous administration of all vaccines for which a child is eligible is very important in childhood vaccination programs because it increases the probability that a child will be fully immunized at the appropriate age.

For some vaccines, administration should not be done at different time intervals. The live parenteral (injected) vaccines (MMR, MMRV, varicella, zoster, and yellow fever) and live intranasal influenza vaccine (LAIV should be separated by at least 4 weeks. This interval is intended to reduce or eliminate interference from the vaccine. The yellow fever vaccine Should be administered less than 4 weeks after the single-antigen measles vaccine. A 1999 study demonstrated that the yellow fever vaccine is not affected by the measles vaccine given 1–27 days earlier. Live vaccines administered by the oral route (oral polio vaccine [OPV] oral typhoid, and rotavirus) are not believed to interfere with each other if not given simultaneously. These vaccines may be given at any time before or after each other. The Rotavirus vaccine is not approved for children older than 32 weeks, and oral typhoid is not approved for children younger than 6 years of age.

Parenteral live vaccines (MMR, MMRV, varicella, zoster, and yellow fever) and LAIV are not believed to have an effect on live vaccines given by the oral route (OPV, oral typhoid, and rotavirus). Live oral vaccines may be given at any time before or after live parenteral vaccines or LAIV. All other combinations of two inactivated vaccines, or live and inactivated vaccines, may be given at any time before or after each other.

 

HIV as the emerging infectious Viral disease

 “Infections that have newly appeared in a population or have existed previously but are rapidly increasing in incidence or geographic range” is termed as Emerging infections (EIs). In 1981, a new disease — acquired immune deficiency syndrome (AIDS)was first recognized. The emergence of HIV raised few questions, firstly the zoonotic source of HIV and its inter and intra species transmission.
Simian immunodeficiency virus (SIV)may have transmitted to humans in at least four separate occasions, identified by individual HIV-1 lineages called groups (M, N, O, P). The most important was the M group of HIV-1, main cause of human infections. HIV-1 is most closely related to SIVcpz, the SIV strain infecting two subpopulations of chimpanzees. Different segments of the SIVcpz genome, are closely related to genome segments of two SIVs of African monkeys, red-capped monkeys and Cercopithecus monkeys.

It is assumed that chimpanzees, regularly kills monkeys, were infected during consumption of their prey; and this infection may have led to a recombination event producing SIVcpz, which was derived from parts of the genomes of the two acquired monkey viruses. Further transmission from Chimpanzee to humans may have occurred during butchering of non-human primates mainly in rural Africa.

During the period from 1930 to 1980 the virus remained as a rare and unrecognized infection in residents of jungle villages in West Africa during this time, reuse of unsterilized needles occurred, a frequent practice during the period of colonial rule, could have helped to spread the virus. 

 

In 1980, the virus began to spread more rapidly. Accelerated spread began in the region centered on Kinshasa (previously Leopoldville) in the Democratic Republic of the Congo (previously the Belgian Congo, then Zaire) and Brazzaville, just across the Congo River in Congo. Transmission was enhanced by the chaos in postcolonial Zaire.
During the period 1985–2004, HIV infection spread widely in Africa. And the prevalence of infection among adults aged 15–49years reached levels higher than 30%. 

The rapid spread was driven by many factors ,such as a high frequency of concurrent sexual contacts in some segments of the population and the hidden nature of sexual networks., the long asymptomatic incubation period during which infected individuals able to transmit the virus were sexually active, the spread along commercial routes of travel within Africa; the failure of health systems to publicize the risks and the under utilization of condoms and other measures to reduce transmission the slow introduction of antiviral treatment after it became available in the northern countries about 1996.

With the spread of HIV in Africa, the M group of HIV-1 evolved into nine different subtypes (A–D, F–H, J, K), based on sequence diversity. Subtype C is most frequent in southern Africa, and subtypes A and D are most frequent in eastern Africa. During the 1980s, HIV spreaded globally, although prevalence rates lower than in some African countries. Subtype B is dominant in the western hemisphere and Europe, while subtype C is most frequent in India and some other Asian countries. Although the global incidence of HIV has fallen slightly since 2010, there are still more than two million new infections each year.

Subacute sclerosing pan encephalitis (SSPE): Persistent measles Virus infection

Subacute sclerosing pan encephalitis (SSPE), also called Dawson’s encephalitis, is a persistent measles infection of the central nervous system. SSPE is a progressive, fatal, encephalopathy characterized by personality changes, mental deterioration, involuntary movements, muscular rigidity, and death. SSPE usually begins 4–10 years after the patient has recovered from naturally acquired measles.
Successful isolation of measles virus from brain and lymphoid tissues of SSPE patients clearly established measles virus as the etiologic agent of the disease. Molecular characterization of measles virus nucleic acid sequences derived from brain biopsy or autopsy has identified wild-type measles sequences with few exceptions, and not those of the vaccine strains.
Measles virus genotypes found in association with SSPE clinical specimens are generally the circulating sequences, in the geographic region where the patients acquired natural infection. No vaccine sequences were identified from tissues of SSPE patients.
SSPE is a very rare but lethal disease, persisting in the human central nervous system (CNS). It is characterized by the absence of viral budding, reduced expression of the viral envelope proteins and spread through the CNS despite massive immune responses. The persistence of measles virus in the brain cells may be due to mutations in the MV genes that were introduced not only due to errors of the MV polymerase, but also in clusters due to hypermutations. The other reasons may be the MV matrix (M) gene, which is most heavily mutated, mutation in the transmembrane glycoproteins, which may be the cause of genetic defects in the persisting measles virus.
The diagnosis is clinical and immunological evidence of measles infection. Management of the disease includes seizure control and avoidance of secondary complications associated with the progressive disability.
Treatment with interferon, ribavirin, and Isoprinosine have reported to give beneficial results. However, the disease shows continuous progression; only 5% of individuals with SSPE undergo spontaneous progress, with the remaining 95% dying within 5 years of diagnosis.